Creatures like sea stars, jellyfish, sea urchins and sea anemones don't have brains, yet they can capture prey, sense danger and react to their surroundings.

So does that mean brainless animals can think?

"Brainless does not necessarily mean neuron-less," Simon Sprecher, a professor of neurobiology at the University of Fribourg in Switzerland, told Live Science in an email. Apart from marine sponges and the blob-like placozoans, all animals have neurons, he said.

Creatures like jellyfish, sea anemones and hydras possess diffuse nerve nets — webs of interconnected neurons distributed throughout the body and tentacles, said Tamar Lotan, head of the Cnidarian Developmental Biology and Molecular Ecology Lab at the University of Haifa in Israel.

"The nerve net can process sensory input and generate organized motor responses (e.g., swimming, contraction, feeding, and stinging), effectively performing information integration without a brain," she told Live Science in an email.

This simple setup can support surprisingly advanced behavior. Sprecher's team showed that the starlet sea anemone (Nematostella vectensis) can form associative memories — learning to link two unrelated stimuli. In the experiment, the researchers trained sea anemones to associate a harmless flash of light with a mild shock. Eventually, the light alone made them retract.

Another experiment showed that sea anemones can learn to recognize genetically identical neighbors after repeated encounters and curb their usual territorial aggression. The fact that anemones change their behavior toward genetically identical neighbors suggests they can distinguish between "self" and "non-self".

A study led by Jan Bielecki, a neurobiologist at Kiel University in Germany, showed that box jellyfish can associate visual cues with the physical sensation of bumping into objects, helping them navigate around obstacles more effectively.

"It is my core belief that learning can be achieved by single neurons," Bielecki told Live Science in an email.

So if animals with nerve nets instead of brains can remember and learn from experience, does that mean they can think?

"This is a tricky question to answer," Sprecher said. The definition of 'thinking' depends on the field. Psychologists, biologists and neuroscientists define 'thinking' differently, Bielecki noted.

Additionally, "thinking is too vague a concept," Bielecki said. Scientists study things like decision-making, pattern recognition, associative learning, memory formation and inductive reasoning. Each has their own, much narrower definition.

Ken Cheng, a professor of animal behavior at Macquarie University in Australia, noted that scientists tend to use the word "cognition" instead of "thinking."

"Scientists shy away from the term 'thinking' because thinking, to most of us, means something running through the head, and we don't have a good way to verify that in another animal or nonanimal species," Cheng told Live Science. Even "cognition" does not have an agreed-upon definition, he said, but "in the broadest sense, cognition is information processing — using information from the world, including the world inside an organism, to do things."

If thinking is that broad sense of cognition, then all life-forms think, Cheng said. This includes animals like marine sponges and placozoans, which process information about their surroundings to keep themselves alive. But when it comes to "advanced cognition," which goes beyond basic learning, however, scientists aren't sure whether brainless animals can think, Cheng said.

Basic cognition can be regarded as any change in behavior that goes beyond reflexes, Sprecher said. By that definition, brainless animals do show cognition. "However, more advanced types of cognitive abilities might require consciousness or self-awareness," he said.

Lotan pointed out that cnidarians (an animal family that includes jellyfish, sea anemones and many other marine invertebrates), which evolved more than 700 million years ago, continue to thrive while many animals with brains have long disappeared.

"This resilience suggests that they possess a unique adaptive system enabling them to endure and flourish through extreme environmental changes over geological timescales — despite lacking a brain," she said. Their neurons allow them to sense and interpret their surroundings, "perhaps representing a rudimentary form of thinking."

Brain quiz: Test your knowledge of the most complex organ in the body

You can use up all the storage on your phone or max out your computer's drive, but can you use up all the memory space in your brain?

Despite how you might feel before an exam or after a sleepless night before a work deadline, neuroscientists say that for a typical, healthy brain, memory capacity isn't fixed or easily used up.

"There isn't a meaningful limit to how much information the brain can store," said Elizabeth Kensinger, a professor of psychology and neuroscience at Boston College. "Memories can be thought of as the data the brain uses to understand the current moment, to make predictions about the future, and to scaffold future learning."

That's because the brain doesn't store memories as isolated files in one specific nerve cell. Instead, a single memory is distributed across many neurons called an engram — a group of brain cells connected and scattered across brain regions. Neuroscientists refer to this pattern, in which a memory is recorded across many neurons, as distributed representation. Each of those individual brain cells plays a role in many different memories.

Consider a memory, such as your 12th birthday party. It is not being stored in a single mental folder. The color of the balloons, the taste of the cake, the sound of your friends singing, and the feeling of excitement all activate different sensory and emotional centers — your visual cortex, taste cortex, auditory system and emotion-processing regions. These areas fire together in a specific pattern, and that pattern of neural activity stores the memory. When you recall that party later, you reactivate the pattern.

This method has significant advantages. Because neurons can participate in numerous combinations, the brain can encode huge numbers of memories. Kensinger suggests related memories share overlapping patterns, helping us to generalize and make predictions — something many neuroscientists believe is the reason for memory. And if a few neurons are damaged, the memory may still be recoverable because it's not stored in just one place.

Paul Reber, a professor of neuroscience at Northwestern University, explained to Live Science that distributed representation is part of what gives the brain its enormous memory capacity. The potential combinations grow exponentially, since each neuron participates in many memories involving overlapping neurons.

Why don't we remember everything?

If the brain isn't limited by memory space, why don't we remember everything? This is because the brain's memory system runs much more slowly than life happens. While information constantly streams in, only a fraction can make it into long-term storage.

Reber suggested thinking of memory like a video camera that only works at 10% of its capacity; we can only remember about a tenth of the specific events, experiences, and encounters we experience.

The information that does get into our memory system is gradually laid down into durable memories that will be there for the long term. That process is called consolidation.

"The storage process is the real bottleneck," Reber told Live Science, "not the total amount of space that you have."

What determines what we keep and what we forget?

At any given moment, tremendous amounts of information come into our brains from all our senses, but we don't need to remember it all.

Human memory did not evolve for perfect recall, Lila Davachi, a professor of psychology and neuroscience at Columbia University, noted. Our memory system evolved for survival, so we prioritize what is helpful so we can navigate the world.

"The memory system is built to only encode what is adaptive and necessary," Davachi, told Live Science.

"We just happened to get so good at it that we have this extra reserve that allows us to reminisce about things that happened when we were in college," Davachi said. "That's not adaptive. I'd argue we don't need it. Why is our memory system keeping that around? Well, it's possibly just an accident."

Kensinger explained that there are efficiencies in how the brain processes and remembers information. "When similar information is encountered over and over again," Kensinger said, "the brain tends to shift from storing the specific details to storing the more general content or schemas of the information. This is an efficient way to store information."

Consider your drive to school or to work. You don't remember every trip, because most of them are similar. Rather than storing each drive as its own memory, you recall the general experience. "The brain will tend to store the details of specific drives only if they had something distinctive happen, Kensinger added," perhaps a road was flooded, or you narrowly avoided an accident."

Far from running out of space, our brains constantly reshape what we know to help us adapt, predict and learn. So the next time you forget where you left your coffee cup, don't worry; you're not running out of space. It's likely your brain just had more important things to remember.

Psychology quiz: What do you know about psychology's most infamous experiments?

How fast do humans think? According to a new study, it's slower than you might expect.

The peripheral nervous system — the network of nerves that deliver information between the brain and the body — takes in environmental information at over a billion bits per second, a speed comparable to a lightning-fast internet connection. But people think and process that information at just 10 bits per second, researchers report in the study.

This vast gulf hints at major unexplored questions in neuroscience and human cognition.

"That number is ridiculously small compared with any information rate we encounter in daily life," the researchers wrote in the study, published Dec. 17 in the journal Neuron. "For example, we get anxious when the speed of the home WiFi network drops below 100 megabits per second because that might compromise our enjoyment of Netflix shows. Meanwhile, even if we stay awake during the show, our brain will never extract more than 10 bits per second of that giant bitstream."

Study co-authors Jieyu Zheng and Markus Meister of Caltech determined this speed limit by calculating the number of bits required to perform a task, such as solving a Rubik's Cube or memorizing the order of a deck of cards, and dividing it by the time it took to perform each task. For record-holding memory experts who can finish those tasks in seconds, the rate at which they processed information was roughly 10 bits per second.

The study raises several questions about how and why human brains filter out all of the extra information taken in by the nervous system. A single neuron can fire fast enough to transmit information at 10 bits per second.

"That one single neuron can perform as well as a monkey," Zheng told Live Science. "You just need one neuron to encode a yes or no decision, and that is enough for you to output that behavior. So why do we need billions of neurons to do this while we still output at 10 bits per second?"

The study also proposes an explanation for why humans can't follow multiple trains of thought at once, like listening to several simultaneous conversations at a party. Evolutionary history may be responsible for this single-minded focus, the researchers proposed. The first nervous systems in early animals were only responsible for guiding an organism toward food or away from danger, so they needed to make only one decision at a time: which direction to move. More abstract thought follows similar "paths" and may have inherited the constraint of processing just one path at a time, the study authors suggested.

The team proposed that the brain operates in two simultaneous modes: an "outer brain" that takes in millions of bits of data and an "inner brain" that focuses on one small portion of that data at a time. To determine how the outer and inner brain communicate with each other, researchers will have to study individuals' brains while they perform complex tasks, such as driving a car, that require people to frequently shift their attention to different aspects of the task, Zheng said.

"How does [the inner brain] do task control?" Zheng said. "How does it choose which 10 bits per second we are paying attention to? We are really hoping that people can go deeper into this."

Disease name: Angelman syndrome

Affected populations: The disorder is believed to affect somewhere between 1 in 12,000 and 1 in 24,000 people, although these figures may be underestimated. Many cases of Angelman syndrome can go undiagnosed because the disorder shares symptoms and characteristics with other conditions. Men and women are equally likely to experience the disorder.

Causes: Angelman syndrome is a genetic disorder named after Dr. Harry Angelman, who first reported it in 1965. The disorder principally affects the central nervous system, meaning the brain and spinal cord, and it's caused by mutations in the UBE3A gene. This gene carries instructions for a protein needed to maintain the normal development and function of cells, including neurons in the brain.

In each cell, humans typically have 23 pairs of chromosomes — thread-like structures that house DNA. One parent contributes half of each chromosome pair, and the other parent contributes the other half. UBE3A is located on chromosome 15. Mutations that delete the gene or change its structure, function or activity can cause Angelman syndrome. In many cases, a mutation develops spontaneously on the copy of the gene from the mother.

The genetic mutations behind Angelman syndrome usually occur randomly, but between 3% and 5% of children inherit them from their parents. In around 10% of people with the condition, the exact cause of the syndrome can't be identified.

Related: New genetic cause of intellectual disability potentially uncovered in 'junk DNA'

Symptoms: People with Angelman syndrome normally start to develop symptoms of the disorder in early childhood. These include developmental problems, such as having difficulty sitting unsupported or babbling, that become apparent around ages 6 to 12 months.

As the disorder progresses, affected people may struggle to speak and walk because of balance and coordination issues. They may also experience seizures, which usually begin when a child is between 2 and 3 years old. Furthermore, some people with the condition may have distinctive facial features, such as a prominent chin, deep-set eyes or abnormally wide mouth. People who have the syndrome usually have a normal life expectancy.

Symptoms of Angelman syndrome can sometimes be confused with other disorders that also cause developmental delays, such as autism or cerebral palsy, possibly leading to misdiagnosis.

Treatments: There is currently no cure for Angelman syndrome.

However, several treatment options exist to help manage their symptoms. For example, doctors may prescribe anti-epileptic drugs to control patients' seizures. Physiotherapy and communication therapy can also help to respectively improve patients' ability to walk and communicate with others without speaking — by using hand gestures or signs, for example.

This article is for informational purposes only and is not meant to offer medical advice.

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Acupuncture relieves pain and improves daily function in people with sciatica better than a sham acupuncture treatment that looks and feels very similar, a clinical trial suggests.

For the new trial, published Monday (Oct. 14) in the journal JAMA Internal Medicine, researchers recruited 220 people with sciatica, a condition that causes pain, weakness, tingling or numbness in the lower half of the body. These sensations are caused by pressure on or damage to the sciatic nerve, the largest nerve in the body; in this case, all of the patients had herniated disks that drove their sciatica.

For people with sciatica, doctors often recommend painkillers, such as over-the-counter drugs like acetaminophen (Tylenol), or prescribe medicines like opioids. Some patients get epidural injections, which are administered into the space around the spinal cord. Some people find relief through physical therapy or self-care practices, like icing or regular stretching. In very severe cases, doctors might recommend surgery to remove the parts of the spine that are pressing on the nerve.

Despite these options, "current treatments for sciatica are unsatisfying," Dr. Jerard Kneifati-Hayek of Columbia University and Dr. Mitchell Katz of NYC Health + Hospitals wrote in a commentary accompanying the new study.

Related: Mindfulness meditation really does relieve pain, brain scans reveal

That's partly because the less-aggressive treatment options don't work for everyone and because the more-aggressive options come with a risk of side effects that deter people from getting the procedures. And even then, approaches like surgery don't relieve every patient's pain.

The new trial provides some concrete evidence that acupuncture may be a helpful treatment option for sciatica. Some past studies hinted that the treatment might be effective, but limitations in their designs prevented scientists from drawing firm conclusions.

By comparison, "this was a methodologically rigorous study," wrote Kneifati-Hayek and Katz, who were not involved in the new trial. They commended the new trial for including experienced acupuncturists, a "well thought-out sham control," and a follow-up period of one year with the participants.

The trial was conducted across six hospitals in China, where all of the participants' diagnoses were confirmed by spine specialists. People with other conditions, such as different spine or neurological diseases, were not allowed to enroll. To be included in the study, all the participants had to have moderate to severe sciatica pain, not be taking any drugs with a therapeutic effect on the condition, nor could they have had acupuncture for sciatica within the past year.

The chosen participants were divided into two equal groups. The first received 10 standardized acupuncture treatment sessions for sciatica over the course of four weeks. The second received a "sham" treatment, in which practitioners placed the needles at "nonacupoints" thought to have no therapeutic effect.

"This is common practice for sham controls in acupuncture research," the study authors noted. In the sham group, most of the needles were placed on the skin but were not actually inserted, with the exception of one needle per session, to help maintain the illusion.

The researchers assessed the participants' subjective experiences of leg and back pain before the treatment began and then a number of times throughout the trial — at weeks two, four, eight, 26 and 52. They also used a questionnaire called the Oswestry Disability Index to check participants' day-to-day function — for instance, how well they could sleep, lift objects and complete personal-care tasks.

The differences between the groups became apparent by week two. Both groups saw reductions in their pain levels and improvements in their daily function, but the true-acupuncture group was faring better at every check-in. "Moreover, the differences between acupuncture and sham acupuncture groups remained statistically significant at week 52," the authors reported.

The sham group may have also experienced pain relief for several reasons, Kneifati-Hayek told Live Science in an email. For instance, because of the placebo effect, or because their symptoms just naturally improved over time, which often happens, he said.

However, the findings still demonstrated that acupuncture treatments provided some benefit "above and beyond" what was seen in the control group, he added.

This persistent result suggests that acupuncture should be considered as a treatment option for people with chronic sciatica from herniated disks, the authors concluded.

That said, the trial did have some limitations. For instance, it didn't directly compare acupuncture to other common sciatica treatments, such as painkillers or surgery. Those direct comparisons would help patients decide which treatments might be the most beneficial for them.

There were no serious side effects that required medical treatment in either group, but the acupuncture group did experience more minor side effects than the sham group did. In all, 26 participants, or 24%, of the real-acupuncture group had a side effect, with minor bleeding and hemorrhage under the skin being the most common. Only five participants in the sham group, or 4.6%, had any side effects related to the treatment.

Going forward, Kneifati-Hayek said that the study supports the idea that acupuncture could be a potentially effective evidence-based treatment for sciatica.

"Studies like this may facilitate the adoption of acupuncture as a form of treatment by health systems and insurers," he said. "It also helps patients and their clinicians make better-informed decisions about approaching sciatica treatment."

This article is for informational purposes only and is not meant to offer medical advice.

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For years, scientists have wondered how migraines can trigger auras — short-lived neurological symptoms that arise before or during migraines. Now, a newly discovered way in which the brain talks to peripheral nerves may be the answer, a mouse study suggests.

More than 1 billion people each year will have a migraine, and about one-quarter of those migraines will be accompanied by an aura. These sensory symptoms can include seeing lights and hearing sounds that aren't there or feeling tingling or numbness. 

Scientists have known that these auras are associated with "cortical spreading depression," waves of abnormal activity that wash over the brain and temporarily inactivate certain neurons. The waves are thought to somehow trip pain-detecting nerves outside the brain, in part by releasing chemicals into the cerebrospinal fluid (CSF), a substance that surrounds and cushions the organ. 

Exactly how the chemicals reached the nerves was a mystery. Now, scientists have uncovered a route by which some molecules can escape the brain's protective barrier. 

Related: Migraines and blood sugar issues share common genetic risk factors

In a study published Thursday (July 4) in the journal Science, researchers examined the route CSF takes to exit the brain by zooming in on a cluster of neurons called the trigeminal ganglion. This bundle of cells transmits signals from the nerves of the face and jaw to the brain, plugging in around the brainstem. 

The scientists discovered that this nerve bundle also provides a route for CSF and the molecules within it to reach the world beyond the brain.

They learned this by using genetically engineered mice whose neurons make a protein that glows in the presence of calcium. Calcium is a key element that brain cells use to send electrical signals. While observing the trigeminal ganglion, the researchers would inject a tracer into the mouse's brain to track the flow of its CSF. They also introduced a substance that allows calcium to flow into neurons, activating them.

The experiment revealed that CSF appeared in the trigeminal ganglion about four minutes after injection, followed by a sharp increase in calcium-driven activity. This provided direct evidence that CSF can carry molecules outside the brain via this channel. 

The fluid likely makes contact with the ganglion near the brainstem. There, the ganglion lacks the tightly fused outer barrier that can be seen elsewhere along its length, the team found.

To connect the dots to migraine, the team looked at the effects of cortical spreading depression. They demonstrated that it can increase the flow of CSF in the affected area, carrying more proteins and other molecules to the trigeminal ganglion than it normally would. Many of those proteins were drivers of pain and inflammation.

"We found that during aura, proteins that can activate and sensitize sensory nerves are released to the CSF and transported to the trigeminal ganglion, where they activate pain-mediating sensory nerves," study author Martin Kaag Rasmussen, a postdoctoral scholar at the University of Copenhagen, told Live Science in an email. 

"This is what drives the migraine headache, and it is what links the aura phase to the headache," he said.

Related: Does caffeine help or cause headaches?

Of the 12 proteins found to activate pain-sensing nerves, only one — calcitonin gene-related peptide (CGRP) — is a current target for migraine therapies. Medications that block CGRP function relieve migraine symptoms in about half of patients, but that still leaves millions of people without effective treatment. 

Rasmussen is optimistic that the additional molecules uncovered in the study could offer new treatment options. "I believe that, when patients do not respond well to currently available therapies, it is because we have not identified what molecule is responsible for their headache," he said. 

"I find it really exciting because it's a new pathway for delivery of molecules from the brain to peripheral ganglia," Andrew Russo, a professor of neurology at the University of Iowa who was not involved in the study, told Live Science. That could have relevance well beyond migraines, he said.

The caveat, however, is that all of the group's experiments were performed in mice. In comparison to the human brain, "the mouse brain is very smooth," Russo said. Humans' brain tissue has more folds so the abnormal waves tied to migraine can't travel as efficiently. That might affect how fast CSF flows out of the brain and whether or not it triggers the pain-sensing nerves, Russo noted.

The next step will be to answer that question by examining the same processes in humans or more human-like animal models. The researchers also want to take a closer look at the new pain-triggering proteins they identified, both in migraines and other headache disorders. This could potentially lead to new diagnostic tests and treatments for a variety of patients.

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A pioneering surgical procedure provides amputees with bionic limbs that are directly controlled by the nervous system, enabling patients to sense the limb's position in space. 

Scientists demonstrated the success of this technique in a new study of seven people who received bionic legs, which was published Monday (July 1) in the journal Nature Medicine. Including these seven, about 60 people worldwide have undergone this type of procedure, which can be used to install either bionic legs or arms. 

"This is the first prosthetic study in history that shows a leg prosthesis under full neural modulation, where a biomimetic gait emerges," Hugh Herr, co-senior study author and a professor of media arts and sciences at MIT, said in a statement. In other words, the synthetic prosthesis is able to fill in for the lost function of the missing limb and thus produce a natural gait.

"No one has been able to show this level of brain control that produces a natural gait, where the human's nervous system is controlling the movement, not a robotic control algorithm," Herr said.

Related: 'You can get the feeling that you are touching another human': New prosthetic device detects temperature

The surgery itself, known as agonist-antagonist myoneural interface (AMI), involves reconnecting muscles in a patient's residual limb after a below-the-knee amputation, in the case that the patient is getting a bionic leg. 

Electrical signals from the central nervous system, which relay instructions for movement, can then pass between these muscles, and be detected by electrodes in a newly installed prosthetic limb. The signals are picked up by a robotic controller in the prosthesis that enables it to control a patient's gait, or way of walking. Signals about the position and movement of a patient's prosthesis are then fed back to the nervous system. 

In a series of experiments described in the new paper, the seven patients who received AMI surgery were able to walk faster than people who received the same type of prosthetic limb, but who had traditional amputations. Some of the patients could even walk at the same rate as people without amputations. They could also avoid obstacles and climb stairs more naturally than patients who underwent traditional amputations. 

Current technology for prosthetic limbs already enables amputees to achieve a natural walking gait, according to the team who conducted the surgery. However, these prosthetic limbs rely on robotic sensors and controllers to actually move in a predefined, algorithmic pattern, the team said. AMI, in contrast, enables the limb to dynamically respond to signals from the body.

"The approach we're taking is trying to comprehensively connect the brain of the human to the electromechanics," Herr said.

The patients who underwent AMI also experienced less pain and muscle atrophy, the scientists reported. 

AMI can also be used for people who have arm amputations, the team said, and the surgery can be done either during a patient's original amputation or at a later date. 

"This work represents yet another step in us demonstrating what is possible in terms of restoring function in patients who suffer from severe limb injury," Dr. Matthew Carty, co-senior study author and an associate professor of surgery at Harvard Medical School, said in the statement.

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Humans have an attuned sense of touch that connects us to our surroundings, and now, scientists think they've discovered a previously unknown way that we use this sense.

A new study has revealed that cells within the outer layer of our hair follicles, the tiny tubes in our skin that surround hair fibers, can detect touch. In response, these cells release chemicals called neurotransmitters that activate nearby sensory neurons, which relay information about our surroundings to the brain. It was previously thought that touch detectors were found only in nerve endings in the skin and near hair follicles — not actually within the follicles themselves.

The findings, published Oct. 27 in the journal Science Advances, were drawn from isolated cells and have yet to be proven in living organisms. However, if confirmed, they may expand the repertoire of known ways that humans sense touch, including via the activation of sensory neurons in the skin that detect both touch and the movement of hair.

"The mechanism we have presented is not better, or more sensitive than direct activation of sensory neurons, which is how we usually process touch," co-senior study author Claire Higgins, a tissue regeneration researcher at Imperial College London, told Live Science in an email.

"So, we are intrigued to discover what the hair follicle adds to the process of touch sensation and why it has this role," she said.

Related: The five (and more) human senses

In the new study, the researchers analyzed the gene activity of more than 40,000 cells isolated from human hair follicles and skin. They did this by looking at RNA molecules, which relay instructions for building proteins from the cell's DNA to its protein construction sites. They found that the hair follicle cells contained three times as many touch-sensitive receptors as the skin cells.

In a separate test, applying tension to human hair follicle cells that had been grown in the lab alongside sensory neurons led to the activation of the latter.

In another experiment, the authors discovered that hair follicle cells activated the nearby neurons by releasing the neurotransmitters serotonin and histamine, which also triggers inflammation. The skin cells also released histamine in response to touch, but not serotonin, and the authors are curious whether both the skin cells' and hair follicles' activation could be linked to skin diseases such as eczema. The skin condition is thought to be exacerbated by histamine-producing immune cells called mast cells, but perhaps these two types of touch detectors also play a role.

"Our work is the first to show that skin cells can also release histamine," Higgins said. "While the levels released are much lower than that released by mast cells, it still suggests a mechanism for skin cells in this disorder," she said.

This research is still in its early days, but as serotonin and histamine can influence each other's production and release in many parts of the body, this could represent a new therapeutic avenue.

"We don't know if this relationship is mirrored in the skin, but if it is, we can explore ways of modulating serotonin as a way to regulate histamine release," she said.

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Neanderthal gene variants may boost the pain sensitivity of people who carry them and may be most common in populations with prevalent Native American ancestry, a new study finds.

The research, published Tuesday (Oct. 10) in the journal Communications Biology, focused on three versions of the SCN9A gene, which codes for a protein that shuttles sodium into cells and helps pain-detecting nerves send signals. People with any of the three variants are more sensitive to pain caused by being prodded with a sharp object, but not pain caused by heat or pressure. 

"In 2020, another group of researchers studied people of European ancestry and linked these Neanderthal gene variants to increased pain sensitivity," first study author Pierre Faux, a geneticist at the French National institute for Agriculture, Food and Environment, told Live Science.

"We extend these findings by studying Latin Americans and showing that these Neanderthal genetic variants are much more common in people with Native American ancestry," Faux said. "We also show the type of pain these variants affect, which wasn't known before."

Related: Mysterious 'Viking disease' linked to Neanderthal DNA

In the new study, the scientists analyzed genetic samples collected from more than 5,900 people living in Brazil, Chile, Colombia, Mexico and Peru. On average, the participants had 46% Native American ancestry, 49.6% European ancestry and 4.4% African ancestry, but these proportions varied significantly between individuals.

The analysis revealed that around 30% of the participants had one of the SCN9A gene variants, called D1908G, while roughly 13% of participants had the other two gene variants, known as V991L and M932L, which tend to be inherited together.

The participants living in Peru, who had the highest proportion of Native American ancestry among the countries studied, were most likely to carry these Neanderthal gene variants. Conversely, participants recruited from Brazil had the lowest proportion of Native American ancestry and were least likely to carry the variants.

"We know that modern humans and Neanderthals interbred something like 50,000 to 70,000 years ago, and that modern humans first crossed over from Eurasia into the Americas by 15- to 20,000 years ago," Faux said.

"The high frequency of the Neanderthal variants in people with Native American ancestry could potentially be explained by a scenario where the Neanderthals carrying these variants happened to breed with the modern humans who eventually migrated into the Americas," he said.

Related: The 1st Americans were not who we thought they were

Following the genetic analysis, the researchers carried out pain threshold tests on more than 1,600 volunteers in Colombia, 56% of whom were women, who had on average 31% Native American ancestry, 59% European ancestry and 9.7% African ancestry. In these tests, participants were asked to tell the researchers to stop as soon as they felt discomfort. The team also analyzed the gene variants carried by each of these tested participants.

In one of the tests, the team applied mustard oil, which irritates the skin, to the forearm skin of participants before pushing plastic filaments of increasing widths onto the same area of skin. In this test, wider filaments exerted a stronger force on the already-irritated skin. Participants who had any of the Neanderthal gene variants tapped out after being prodded with filaments that were significantly smaller than those who did not carry the gene variants.

"When we tested the participants' pain threshold by applying pressure, heat or cold, the gene variants did not affect pain sensitivity, so the Neanderthal variants only affected their response to pinprick pressure," Faux noted.

It is possible that carrying these gene variants gave Neanderthals, and the modern humans who first settled the Americas, some sort of survival benefit, Faux said. But that survival benefit wasn't necessarily related to pain sensitivity, he added.

"The modern humans who first reached North America would have had to bear harsh and cold conditions, so it could be that these variants have other effects beyond pain — for example, they could have somehow helped humans to cope with the cold," he said. In other words, the heightened sensitivity to sharp objects might have been just a side effect of another evolutionary change.

However, the evolutionary pressures that acted on SCN9A were likely complex, and "why Neanderthals might have had a greater pain sensitivity and whether introgression in SCN9A represented an advantage during human evolution remains to be determined," the authors wrote..

Nevertheless, it is interesting to know these gene variants, which have previously been linked to small fiber neuropathy — a painful nerve condition — would have also caused pain in our Neanderthal ancestors, Sulayman Dib-Hajj, a professor of Neurology at the Yale School of Medicine who was not involved in the study, told Live Science in an email.

It's a familiar feeling: Before a test, a first date, or a public speaking engagement, your stomach starts to "flutter" as if butterflies were flying around inside your gut. Stomach sensations are a common side effect of being nervous, and they may also manifest as a feeling of a "knot" or even as more severe digestive symptoms.

But where do these feelings actually come from?

It turns out, a "nervous stomach" is one of the best examples of the two-way connection between the digestive system and the nervous system.

"From the earliest stages of embryonic development, the brain, spinal cord and digestive tract are all tightly wired to each other," Melissa Hunt, a clinical psychologist at the University of Pennsylvania, told Live Science in an email. "Millions of neurons send information from the gut back to the brain, and just as many neurons send signals back to the gut."

This link is often referred to as the gut-brain axis. It's modulated by hormones and neurotransmitters — chemical messengers that respectively have broad effects via the bloodstream or act locally between nerve cells. It is also controlled by direct nerve connections between the brain and gut? and even by bacteria, and it's one reason your mood can so often affect the rest of your body, and vice versa.

"When we feel "butterflies" in our stomach, it's a vivid reminder that our emotions are deeply embodied," John Cryan, a professor of anatomy and neuroscience at University College Cork in Ireland, told Live Science in an email. "Ultimately, butterflies in the stomach illustrate the gut-brain axis in action: a continuous, bidirectional conversation between the central nervous system and the gut through neural, hormonal, and microbial pathways."

How the gut-brain axis creates butterflies in your stomach

The nerve cells that line the gastrointestinal tract are part of the "autonomic" nervous system, which regulates involuntary bodily functions, such as breathing, heartbeat and digestion. When food enters the gut, for example, its resident nerve cells prompt muscle cells to contract and push the food through the intestines, according to Harvard Health.

The autonomic nervous system is divided into two branches: the parasympathetic nervous system and sympathetic nervous system. These systems, respectively nicknamed the "rest and digest" and "fight or flight" systems, balance each other out. In general, the parasympathetic nervous system relaxes the body, while the sympathetic nervous system bolsters its response to danger.

When you're feeling anxious, the fight-or-flight response is activated. In this state, the body releases stress-related hormones, such as cortisol, that suppress digestion processes in the stomach and small intestine; meanwhile, other hormones actually stimulate the large intestine. These simultaneous changes cause muscle contractions that can feel like "butterflies" in the stomach, and they can also cause more severe digestive distress, such as nausea, bloating, constipation or diarrhea.

While these feelings often seem like an annoyance or inconvenience today, they may have once played a pivotal role in human life.

"From an evolutionary standpoint, this reaction likely helped our ancestors survive," Cryan explained. "Shutting down digestion and diverting resources toward immediate physical readiness would have improved chances of escape or confrontation. The gut sensations that accompanied these shifts also served as internal cues, highlighting moments of high importance or uncertainty."

You may have heard that the microbiome — the community of microorganisms that live in and on our bodies — plays a big role in the gut-brain axis. And that holds true for the sensation of a nervous stomach, too.

"Although the gut microbiome doesn't cause the flutter directly, it helps shape how strongly we experience and recover from such sensations," Cryan said. The bacteria in our guts may secrete substances that influence gut-brain signaling, and this, in turn, could affect how strongly someone feels a fluttery stomach.

"A healthy, diverse microbiome may buffer overactive stress responses, while alterations in microbiome composition can heighten them," Cryan suggested. The interactions between the microbiome and the gut-brain axis are still a relatively new area of research, and scientists are still determining how specific microbes influence gut-brain signaling.

Two-way road

Just as stress can trigger a nervous stomach, frequent gastrointestinal (GI) problems can also cause stress, Harvard Health notes.

What's more, stress can increase the frequency or severity of symptoms in "disorders of gut-brain interaction," or DGBIs. This umbrella term covers GI conditions that cause significant symptoms and impact quality of life but don't always trigger clear, measurable changes in the digestive tract. These include conditions like irritable bowel syndrome (IBS), in which a variety of symptoms, such as abdominal pain, diarrhea or constipation, occur without a clear cause; or functional dyspepsia, which involves stomachaches that occur during or after eating, without a known cause.

DGBIs are thought to be characterized by ongoing disturbances in communication between the gut and the brain, as well as shifts in the gut microbiome and immune function, in some cases. Over time, people can become anxious and hypervigilant about their GI symptoms, Hunt noted.

"This leads to visceral hypersensitivity, which becomes a vicious feedback loop of anxious arousal, scanning the body for uncomfortable sensations, catastrophizing, amplification of those sensations, which increases anxiety and then leads to increased GI discomfort and distress," she said.

That's why behavioral therapy is sometimes incorporated into patients' treatment plans for DGBIs, to help break this cycle.

"Far from being 'just in your head,' emotional experiences are woven through your viscera," Cryan said. "Understanding this connection reminds us that mental and digestive health are inseparable."

This article is for informational purposes only and is not meant to offer medical advice.

A sea animal so simple that it looks like a blobby pancake may hold the secret to the origin of neurons.

Placozoans are one of the five major branches of animals, along with bilaterians (which include everything from worms to humans), cnidarians (corals and medusas), sponges and ctenophores (comb jellies). They're the most basic of the bunch, consisting of millimeter-long blobs of cells without organs or body parts. They move through the water using cilia — tiny hair-like structures — absorb nutrients by engulfing particles, and reproduce by simply budding off new offspring.

Placozoans diverged from other animals about 800 million years ago, and just a few species are known. But new research has found that these unassuming creatures may hold the key to the eventual evolution of the nervous system. Placozoans, it turns out, contain cells that show striking similarities to neurons, even though they are nowhere near as complex.

"Our results fit into the idea that neurons are a very complex cell type that has evolved in a gradual way," study author Xavier Grau-Bové, a postdoctoral researcher at the Centre for Genomic Regulation in Barcelona, told Live Science. "We are maybe seeing the remnants of something that, when we diverged with placozoans, was sort of an ancestral neuron with likely a different function."

Related: Decades-old question surrounding the start of the tree of life could finally be solved

Grau-Bové and his colleagues embarked on a systematic genetic study of all the cell types in placozoans. The cell biology of these little organisms has only rarely been studied, he said: "We are starting from virtually nothing."

The researchers mapped out nine main cell types and several intermediate cell types, but the most intriguing turned out to be a subset called peptidergic cells. These cells contribute to placozoans' movements by releasing short chains of amino acids called peptides. Stimulation with different peptides causes placozoans to change their shape and movement; for example, they might flatten, undulate or crinkle up, according to 2018 research.

The peptidergic cells showed surprising similarities to the neurons that make up the nervous systems of animals like humans. In particular, they have the proteins that build what scientists call the "pre-synaptic scaffold." Neurons communicate by releasing chemicals across a gap called a synapse. Peptidergic cells don't have synapses — but they do have similar protein complexes to those in neurons that enable chemicals to build up and then be released.

"We do not yet know exactly what this scaffold is doing in these organisms," Grau-Bové said. "We just know that it is being expressed there."

The team found that these peptidergic cells developed in a similar way to neurons. They also observed cell-to-cell messaging using neuropeptides, which are amino acid chains used by neurons in their own messaging systems.

The origin of neurons remains a controversial question among biologists. Sponges don't have them, and comb jellies have neurons that look extremely different from other animals', while cnidarian and bilaterian nervous systems have more in common. It's not clear whether the common ancestor of all these animals had a nervous system and then some lineages, like sponges, dropped it, or if the nervous system evolved separately in multiple lineages after they diverged from one another.

More studies on ctenophores and their oddball nervous systems will be necessary to answer that question, Grau-Bové said, but the new research suggests a slow-and-steady evolution of neurons from a simpler cell specialized for communication and messaging.

The results were published today (Sept. 19) in the journal Cell. 

If you miss your morning cup of joe, your temples may start throbbing. If you drink more than normal, that could cause a headache, too. And somehow, a strong cup of coffee can also stop some migraines in their tracks. 

So is caffeine the culprit or the cure for headaches? Is the problem too much or not enough? The answer: all of the above. 

The key to understanding caffeine is to remember that it's no ordinary ingredient. Caffeine is a psychoactive substance, said Dr. Richard Lipton, a professor of neurology at Albert Einstein College of Medicine in New York City. It has stimulating and vasoconstricting properties, meaning it speeds up brain activity and causes veins in the head to narrow, which help explain caffeine's roles in headaches — both as instigator and reliever. 

Related: Does coffee really give you an 'energy boost'? 

Caffeine as headache treatment 

Caffeine's ability to relieve a withdrawal headache or halt a migraine is well established; it's a key ingredient in multiple over-the-counter and prescription drugs, including headache-specific medicines like Excedrin. 

"It's not a pain reliever in its own right, but when combined with pain relievers, it makes them more effective," Lipton told Live Science. While caffeine's synergy with pain relievers is not fully understood, it could be related to caffeines activity in the brain.

The caffeine molecule binds to adenosine receptors in the brain and spinal cord. Normally, adenosine, a building block in DNA's molecular cousin RNA and in the main chemical fuel used by the body's cells, binds to these receptors, but it's blocked by ingested caffeine.  

By taking up the seats adenosine would normally occupy, caffeine blocks the molecules' effects. While adenosine slows nerve activity, caffeine increases it. Adenosine increases blood flow and causes blood vessels to widen, while caffeine constricts them; as some headaches partly stem from vasodilation in the head, caffeine's role as a vasoconstrictor may partly explain its effects. 

However, adenosine also plays a complex role in pain transmission, sometimes quelling pain signals and sometimes promoting them, so caffeine may also relieve headaches by messing with this signaling. Studies also show that, when taken with caffeine, pain relievers like acetaminophen are absorbed faster and their effects may last longer. In a study in which providers and patients didn't know whether they received an active pill or a placebo, caffeine with ibuprofen provided better and faster pain relief than ibuprofen alone.

However, caffeine's pain-killing abilities vary widely depending on how much people normally consume, according to Stanford Health Care. People develop a tolerance with frequent caffeine use and can then become dependent on caffeine's effects. This minimizes its headache-relieving effects. 

Related: What are the different types of headaches? 

Not enough or too much

On the flip side, caffeine can also cause headaches — both when people consume less than they normally would and when they consume too much. 

In the former case, headaches can occur because, with daily use, caffeine starts to change the brain's structure. "When your receptors are chronically exposed [to caffeine]," Lipton said, "then your brain doesn't function normally unless the caffeine is around."

Studies suggest that regular caffeine consumption increases the number of adenosine receptors in a person's brain, making a person more sensitive to adenosine's effects. Withdrawal headaches occur because the body becomes used to the vasoconstriction that comes with daily caffeine, and without it, those blood vessels suddenly swell, which can cause headaches. 

The good news is that once you catch up on your caffeine, these headaches usually go away — or after a period free from caffeine, the brain's number of adenosine receptors falls, as do the symptoms of withdrawal. 

Excess caffeine can also trigger headaches. Headache is one of the many side effects of caffeine overdose, and for some migraine patients, caffeine can actually trigger an attack. However, while there's rigorous evidence behind caffeine withdrawal headaches and caffeine's benefits in combination with painkillers, the reason excessive caffeine causes headaches is less established, Lipton said. But it's a phenomenon neurologists like Lipton have observed in the clinic, he said. 

To be safe, the Food and Drug Administration says healthy adults should limit their caffeine intake to 400 milligrams — the equivalent to four or five cups of coffee — per day.  But it's important to note that individuals' sensitivity to caffeine can vary. 

"Caffeine is definitely this two-edged sword," Lipton said. It can be mood-boosting and productivity-enhancing, and sometimes pain-stopping, but overuse and overdependence are fast paths to a throbbing headache. 

This article is for informational purposes only and is not meant to offer medical advice.

People with heart disease often develop dreadful sleep problems, and now, scientists have identified a direct link between these conditions for the first time in a new study in mice and human tissues. 

Published Thursday (July 20) in the journal Science, the research shows that heart disease may derail the production of the sleep hormone melatonin in the brain due to damage to a group of nerves that innervate, or plug into, both organs — the superior cervical ganglion (SCG).

Found in the neck, these nerves are part of the autonomic nervous system, which regulates involuntary processes in the body, such as breathing and heart rate. Because nerves originating from the SCG connect to both the heart and the pineal gland — the tiny brain structure responsible for melatonin production — issues with the heart could explain why the body's melatonin-maker falls off track. 

"Imagine the ganglion as an electrical switchbox," senior author Stefan Engelhardt, a professor of pharmacology and toxicology at the Technical University of Munich, said in a statement. "In a patient suffering from sleep disturbances following a heart disease, you can think of a problem with one wire causing a fire to break out in the switchbox and then spreading to another wire."

Related: Irregular sleep may increase your risk of dying from cancer and heart disease 

The research is "important and timely," Brooke Aggarwal, an assistant professor of medical sciences at Columbia University who was not involved in the study, told Live Science in an email, noting that it "suggests a novel mechanism that may help to explain why those with heart disease are more prone to sleep disturbances." 

She went on to caution, though, that "future prospective studies need to be conducted, as well as clinical trials of any potential treatments stemming from this mechanism."

Struggling to sleep is a common side effect of heart disease — for example, up to 73% of people with heart failure experience symptoms of insomnia. Past studies have shown that melatonin levels are reduced in people with heart disease, but scientists didn't know why. 

In the new study, researchers analyzed human brain tissue samples from deceased heart disease patients and from people without heart disease. This postmortem analysis revealed a reduced number of nerve fiber, or axons in the SCG of people who had heart disease compared with the "heart-healthy" control group. The SCG of the individuals with heart disease were also markedly scarred and enlarged.

In supporting mouse experiments, the team found that immune cells called macrophages, which gobble up diseased and damaged cells, were present in the cervical ganglia of mice with heart disease, and the rodents' nerves showed signs of inflammation and scarring. The mice also had fewer axons in their pineal glands and less melatonin in their blood than healthy mice did. The rodents' circadian rhythms — the internal processes that regulate how the body responds to day and night — were also disrupted, as evidenced by changes in their metabolic rates and activity levels, for example.

Giving mice melatonin completely reversed this disruption, the team found. Additionally, when drugs were used to destroy the macrophages in the rodent's SCGs, their melatonin levels were restored.

Because these analyses were conducted in mice and only 16 humans, the findings "call for further studies" to reveal the mechanisms that drive immune cells to the SCG, the researchers noted in the paper. This may involve studying the nerve cells that link the heart and spinal cord, as well as messenger proteins called cytokines that summon macrophages.

In time, the team believes the study may pave the way for the development of new drugs to treat sleep disturbances caused by heart disease. 

"It will be now pivotal to obtain evidence in a randomized clinical trial to determine whether therapeutic melatonin is indeed effective in treating sleep disorders in patients with chronic heart disease," Engelhardt told Live Science in an email. If it proves effective, "then this could spare many patients the unnecessary side effects that come with standard sleeping pills."

Ctenophores, or comb jellies, are strange jelly-like animals that ghost through the sea propelled by tiny hairs called cilia. They're an enigmatic bunch, with origins that stretch back approximately 540 million years, and no one is sure exactly when they diverged from the rest of the tree of life. 

Now, researchers have discovered that these alien-like creatures are even weirder than we thought: Their nervous system is like nothing ever seen before. Instead of relying on gaps between nerve cells called synapses for communication, at least part of the ctenophore nervous system is fused. 

"We haven't actually seen this in any other animal before," study co-author Maike Kittelmann, a cell and developmental biologist at Oxford Brookes University in the U.K., told Live Science. "It means that there are other ways that neurons can connect to each other." 

Nervous system evolution

The discovery raises questions about how all nervous systems evolved and adds fuel to a long-standing debate about how comb jellies are related to the rest of the animal kingdom. Many scientists thought that the nervous system in animals evolved only once, at some point after sponges broke off from the rest of the animal kingdom, as sponges do not have a nervous system. But some scientists think ctenophores diverged from other animals early and evolved their own nervous system separately. 

Related: What's the weirdest sea creature ever discovered?

Comb jellies don't have brains, but have a weblike system of neurons known as the nerve net. It's within this nerve net that researchers found the fused neurons. The strange fused arrangement could hint that these systems evolved independently, Kittlemann said. But it's still an open question. 

"We don’t really know for sure," she said. 

The new research, published April 20 in the journal Science, looks at ctenophores in an early developmental stage, when they're just a few days old. At this stage, ctenophores can move around freely and even reproduce, but they're not full adults. (Depending on species, ctenophores have life spans between about a month and several years.)

The vast majority of nerve cells in animals communicate via synapses, which are gaps between cells. To "talk," neurons release chemicals called neurotransmitters across these gaps. But the new study found that within the ctenophore nerve net, the cells are fused and their membranes connected so that the path from cell body to cell body is continuous. This structure is called a syncytium. 

"There are some other animals which show fused neurons but not to that extreme, where you have a whole nerve net," study co-author Pawel Burkhardt, who studies the evolutionary origin of neurons and synapses at Norway's University of Bergen, told Live Science. 

Fused neural networks

The discovery raises a whole bevy of new questions, Burkhardt said, from how this fused network develops to how it functions. The same cells that are fused together also make connections to other nerve cells via synapses, and other parts of the ctenophore nervous system use synapses, too. It's not clear, Burkhardt said, why comb jellies use two different methods of communication between their nerve cells. 

One possibility is that the fused nervous system has some advantage for tissue repair and healing, Leslie Babonis, an evolutionary biologist at Cornell University who was not involved in the new study, told Live Science. Ctenophores are capable of regenerating an entirely new animal from a small chunk of flesh. 

"Maybe this is one of the secrets to their incredible ability for regeneration," Babonis said.

The research team only looked at one species of ctenophore — Mnemiopsis leidyi — in one developmental stage, so they now plan to find out whether other species have fused neural networks and whether this fusion persists through the animal's whole lifespan. 

This could help answer questions about the evolution of the nervous system and whether it arose once, twice or more times. If many ctenophores have unique fused nervous systems, this could lend credence to the hypothesis that ctenophores evolved their nervous system separately from other animals. But it's also possible that all animal nervous systems still share a common origin, and ctenophores evolved the fusion later, the researchers said. 

Only a handful of lineages in the animal kingdom have had their nervous systems closely studied, Leonid Moroz, a biologist at the Whitney Laboratory for Marine Biosciences at the University of Florida, told Live Science. Moroz was not involved in the current study but led a 2014 study of ctenophores, which found that the genetic and chemical basis of the ctenophore neural system is quite different from that seen in other animals.

If the nervous system is a poem, Moroz said, ctenophores use a different alphabet from the rest of the animal kingdom to write theirs. He argues that these jellies evolved their nervous system independently, and that other understudied animals may have done the same. Unraveling this diversity could lead to a deeper understanding of how neurological disorders arise. 

"We need to understand syntax, we need to understand grammar," Moroz said. "But we cannot do it with only one or few species." 

Scientists may finally have an explanation for why poor sleep is tied to chronic pain. A new mouse study suggests that nerve injuries make certain brain cells go haywire during sleep, and this sudden excitement may lead to chronic pain. Conversely, stopping the hyperactivity during sleep can help relieve the pain, the study hints.

People with chronic pain often experience sleep disorders, including insomnia, and evidence suggests that poor sleep quality is a major risk factor for developing chronic pain in the first place. Although this link is well-established, "the nature of the sleep problems for different pain conditions, their precise causes or their long-term consequences are yet unknown," said Alban Latremoliere, an assistant professor of neurosurgery and neuroscience at the Johns Hopkins School of Medicine, who was not involved in the new study. 

"You will often hear about the 'vicious circle' whereby pain disrupts sleep, which in turn worsens pain, but the biological pathways involved have been extremely elusive," Latremoliere told Live Science in an email. The mouse study, published Monday (Jan. 23) in the journal Nature Neuroscience, starts to unravel the inner workings of one of these mysterious pathways, he said. 

The study focused on neuropathic pain, which arises from an injury or disease in the nerves that relay sensory information from the body to the brain. The researchers studied mice with injuries in one of the sciatic nerves, the major nerves that extend from the spinal cord to the hind legs. Two of the nerve's three branches that plug into the leg were injured, and this caused the skin supplied by the remaining branch to become hypersensitive, explained Guang Yang, senior author of the study and an associate professor of anesthesiological sciences at the Columbia University Irving Medical Center in New York City. 

Related: Can you make up for lost sleep?

"It mimics human neuropathic pain related to peripheral nerve injury," Yang told Live Science in an email.

The team analyzed the rodents' brain activity before and after injury and spotted distinct changes in the region of the wrinkled cerebral cortex that receives sensory data from the hind leg. Brain cells with pyramid-shaped bodies, aptly named pyramidal neurons, became progressively more active in the weeks after injury, as the mice's pain entered the chronic phase. But their hyperactivity peaked during non-rapid eye movement sleep (NREM), when deep sleep occurs.

Why did these pyramidal neurons go haywire? The team traced the blame back to the anterior nucleus basalis, a cluster of neurons lodged deep in the front of the brain. 

The activity of this cell cluster had also increased after injury, the team found, and this led the cells to send the chemical messenger acetylcholine up to the cerebral cortex. Through a chain reaction, this action essentially lifted the breaks off the pyramidal neurons, shifting them into overdrive.

This shift in brain activity was linked to a change in pain sensitivity in the mice, where once-painless stimuli suddenly became painful. In a series of experiments, the researchers found that they could relieve this pain by blocking the hyperactivity of different cells in the brain pathway they'd discovered. 

"Inhibition of this pathway during NREM sleep, but not wakefulness, corrects neuronal hyperactivation and alleviates pain," the researchers wrote in the study.

Eventually, this line of research could lead to new treatments for humans with chronic pain, but this initial study is somewhat limited because it's in mice. 

"While I believe the same problems observed in mice are likely to occur in humans, their exact profile and distribution might vary in patients," partially because humans' circadian rhythms differ from those of the nocturnal rodents, Latremoliere said. He added that he'd be interested in seeing whether this newfound pathway contributes to other types of chronic pain, such as cancer- or chemotherapy-related pain.

Yang and her colleagues aim to study whether their results carry over to humans. The current study raises the idea that chronic pain may be "encoded" in the brain during sleep, not unlike how memories are built into the brain during sleep, she told Live Science.

"The knowledge that neural circuit remodeling during sleep plays such a vital role in the formation of chronic pain is highly relevant to pain therapeutics," she said.

Whether it’s a nervous sensation in the stomach before an important presentation or "butterflies" at the sight of a loved one, many people are aware of the connection between the gut and the brain. But the gut-brain axis is a real phenomenon, describing a two-way communication between the central nervous system (CNS) and the enteric nervous system (ENS). 

But with several different communication methods in both directions, scientists are still establishing exactly how it works. Here, we've unpacked some of the potential mechanisms behind the gut-brain axis and their implications for mental health. 

What is the gut-brain axis?

Grace Derocha, a registered dietitian in Chicago and a national spokesperson for the Academy of Nutrition and Dietetics, said that the gut-brain axis is a two-way communication that takes place between the gastrointestinal tract and the central nervous system.

"It links emotional and cognitive centers of the brain with intestinal functions," she said. "A troubled gastrointestinal tract can send signals to the brain, just as a troubled brain can send signals to the gut." 

This gut-brain communication happens through a sophisticated network with multiple pathways. Here are some of them.

Chemicals produced by gut microbes

Jane Foster, a professor of psychiatry at UT Southwestern in Texas, said that a key player within this communication system is the gastrointestinal tract, home to trillions of microbes.

A person's diet has a significant impact on these microbes. Fiber, for example, is fermented by gut bacteria, which produce metabolites called short-chain fatty acids. These include butyrate, propionate, and acetate. According to a 2020 study, published in the journal Molecular and Cellular Neurosciences, short-chain fatty acids have the power to cross the blood-brain barrier, where they can impact brain structure and function.

Inflammation

"The immune system is part of the gut-brain axis and is an important signaling cascade from microbes to the brain," said Foster.

An imbalance in gut bacteria — known as dysbiosis — causes the barrier between the gut and the bloodstream to become permeable. This can allow "bad" bacteria to enter the bloodstream, potentially causing inflammation. A 2020 review, published in the journal Frontiers in Immunology, suggests that dysbiosis also alters the blood-brain barrier, contributing to inflammation of the brain matter. Inflammatory pathways have been linked to neuroinflammatory conditions including multiple sclerosis, Alzheimer’s and Parkinson’s diseases, as well as anxiety and depressive-like disorders. 

The vagus nerve

The human gut contains nearly 500 million neurons which are connected to the brain through nerves. The vagus nerve is one of the biggest nerves connecting the gastrointestinal tract to the nervous system and plays many important roles in the body.

Psychological stress, for example, may have a particularly harmful effect on the vagus nerve, with a 2014 study, published in the journal PLOS One, finding it may be involved in the development of gastrointestinal disorders like irritable bowel syndrome and inflammatory bowel disease. 

Neurotransmitters

The gut and the brain also communicate through chemicals called neurotransmitters. Some of these neurotransmitters are produced in the brain and are involved in regulating emotions, mood and the "fight or flight" response.

They can also be produced in the gut, affecting aspects of digestive, according to a 2016 review published in the Journal of Cellular Physiology. It found that neurotransmitters including norepinephrine, epinephrine, dopamine, and serotonin are able to regulate and control blood flow and affect bowel movements, nutrient absorption and the composition of the microbiome.

Gut-brain axis and mental health: What’s the link?

Whilst there is emerging research, we're only just beginning to understand the nature of the relationship between the gut-brain axis and mental health. Much of the evidence is based on animal research, so it is hard to draw conclusions about how this translates to humans.

It's also hard to establish cause and effect when it comes to the relationship between the gut and the brain.

"A person's intestinal distress can be the cause or the result of anxiety, stress, or depression," said Derocha.

Diversity and balance are hallmarks of a healthy gut microbiome. Research suggests there might be links between the types of microorganisms in a person's gut and their mental health.

"The microbiome of a person with a mental health problem is different from a healthy person," said Foster. "Alzheimer's disease and Parkinson's disease are [also] linked to a different profile of microbes in the gut."

A 2021 review, published in the journal Pharmacological Research, suggests that poor gut health may contribute to the onset and progression of mental health conditions, including depression and anxiety. In patients suffering from depressive disorder, levels of Enterobacteriaceae and Alistipes ("bad" bacteria) were enhanced, whilst the level of Faecalibacterium ("good" bacteria) was reduced. The researchers also found that there was less diversity in gut bacteria in patients with mental disorders, as well as a decrease in bacteria producing short chain fatty acids. However, again, it is not clear whether changes in gut bacteria influence mood disorders or vice versa. 

Nutrition and mental health

Probiotics — beneficial bacteria found in fermented foods and dietary supplements — can support gastrointestinal health, according to a 2016 meta-analysis published in the journal PLos One. A promising new field known as psychobiotics is considering the role that probiotics could play in alleviating mental health symptoms. However, further research is needed.

Cognition and memory

Emerging evidence identifies a correlation between the gut microbiome and cognitive performance. A 2017 study, published in the Journal of the International Neuropsychological Society, found a link between gut microbiome composition and cognition in older adults. Individuals with lower proportions of Bacteroidetes and Proteobacteria and higher proportions of Firmicutes and Verrucomicrobia performed significantly better on tests associated with attention, learning and memory. 

This article is for informational purposes only and is not meant to offer medical advice.

You're engrossed in a mystery novel, but in your excitement to discover "whodunit," you turn the page too quickly and slice open the skin of your pointer finger. A jolt of pain shoots through the paper cut and you gasp, not because you've just learned that the butler did it, but because the teeny-tiny cut hurts so badly.

Why are paper cuts so painful? 

It's a combination of our hands being incredibly sensitive to pain and papers' edges being surprisingly jagged.

Human hands and fingers carry a high concentration of nerve cells called nociceptors, which respond to signals released by damaged cells, according to BrainFacts.org. Paper cuts primarily set off "mechanical nociceptors," which sense cell damage caused by pressure, cuts and punctures, as opposed to damage caused by extreme temperatures, for example. To a lesser extent, paper cuts can also activate nociceptors that are sensitive to chemical irritants, such as the bleaches used to lighten paper; these nerve cells may generate sensations of itchiness around a paper cut.

Activated nociceptors let loose a flurry of electrical signals that travel through bundles of nerve fibers and into the spinal cord; nerve cells in the spinal cord then relay those signals to the brain. Ultimately, the signals reach a region of the wrinkled cerebral cortex responsible for sensations of touch, temperature and pain, known as the somatosensory cortex, according to the medical resource StatPearls.   

Related: The five (and more) human senses 

The somatosensory cortex curves over the brain's surface like a headband, with different regions of the headband representing different body parts.Hands and fingers are so packed with touch- and pain-sensitive cells, so  regions of the headband dedicated to them are enormous compared with those of less-sensitive body parts, like the trunk. The mouth and tongue take up a similarly expansive region of the headband, which helps explain why slicing open your tongue while licking an envelope is also super painful.

But it's not just anatomy that makes paper cuts oddly painful; the paper itself also adds to the agony. Although it looks smooth to the naked eye, at a microscopic level, the dried, compressed wood fibers within paper make the materials' edges quite rough, according to Cosmos. This rough texture causes more extensive cellular damage than a straight, clean edge would. 

That said, paper's serrated edge typically only slices through the top two layers of skin — the epidermis and dermis — and therefore causes little to no bleeding. This lowers the likelihood that the cut will become sealed with clotted blood. As a result, the aggravated nerve fibers remain exposed to the elements for a prolonged period of time and shoot off pain signals whenever touched.        

To treat a paper cut, clean the wound with soap and water; apply antibiotic ointment to prevent infection; and cover it with a bandage to provide cushion and block out debris, according to The Ohio State University Wexner Medical Center. Most paper cuts heal within two to three days, but if the cut doesn't improve in that time, it's best to see a doctor and have them check for signs of infection. 

You're rounding a corner in your home when a jolt of pain suddenly shoots through your pinky toe. You let out a yelp and find yourself frozen to the spot, desperately waiting for the throbbing in your stubbed toe to subside.

There's no pain quite like ramming your toe into a door frame or table leg, although the resulting injury is typically minor. So why does stubbing your toe hurt so much in the moment? The answer comes down to the quantity and type of nerve fibers in the feet and the force with which you typically stub your toes.

Painful sensations in the body originate in nerve cells called nociceptors, whose fibers plug into the skin, muscles and internal organs and respond to signals released by damaged cells, according to BrainFacts.org. 

Different types of nociceptors respond to different types of damage. Touching a scalding-hot pan sets off thermal nociceptors, for example, while stubbing your toe activates mechanical nociceptors, which are sensitive to pressure, cuts and wounds. 

Related: The five (and more) human senses 

When activated, mechanical nociceptors shoot a message from the free nerve endings in your stubbed toe to dense bundles of nerve fibers that feed into the spinal cord. From there, the signals zip up to the brain and pass through an information hub called the thalamus before being forwarded to the wrinkled cerebral cortex.     

The part of the cortex that responds to signals indicating touch, temperature and pain curves over the brain, sort of like a headband, and different areas of the headband process sensation in different body parts, according to the medical resource StatPearls. 

The specific region that deals with the feet and toes lies at the headband's center, where the two halves of the brain meet, and its size reflects the number of receptors in the feet. The ultrasensitive face, mouth and hands take up the most space in the sensory headband, but the feet still take up a lot of real estate compared with the less-sensitive trunk and limbs. 

Not all pain-related signals from a stubbed toe reach the brain at the same time, according to Stanford Medicine's Scope blog. 

The initial lightning bolt of pain triggered by the stubbing is relayed by "A-delta fibers" — thin, fat-encased nerve fibers that send signals super efficiently. The dull, aching pain that emerges seconds later arises from less-efficient "C fibers," which have nerve endings that cover a wide area, meaning several toes rather than the tip of one. This pain can worsen if the injury triggers inflammation.

Nociceptors in the feet can be particularly sensitive to physical trauma, like toe-stubbing, because the feet carry little fat that could help soften the blow, Insider reported. What's more, when you stub your toe, you're likely hitting these vulnerable nerve fibers with a force equal to two to three times your body weight, and all that force is concentrated on a tiny surface area.

Thankfully, the intense pain triggered by stubbing your toe usually resolves within minutes or hours. However, in a minority of cases, a stubbed toe can result in more serious tissue injury, like a sprain, or even broken bones or dislocated joints, according to the Cleveland Clinic. If the pain remains severe for days and worsens when you attempt to move your toe, it can be a sign of more serious injury. 

People with paralyzing spinal cord injuries can walk again with the help of medical devices that zap their nerves with electricity. But the designers of these new implants weren't completely sure of how they restored motor function over time — now, a new study provides clues. 

The new study of humans and lab mice, published Nov. 9 in the journal Nature, pinpoints a specific population of nerve cells that seems key to recovering the ability to walk after a paralyzing spinal cord injury. With a jolt of electricity, an implant can switch these neurons on and thus jumpstart a cascade of events in which the very architecture of the nervous system changes. This cellular remodel restores the lost lines of communication between the brain and the muscles needed for walking, allowing once-paralyzed people to walk again, the researchers concluded.

Understanding how the nerve-zapping system, called epidural electrical stimulation (EES), "reshapes spinal circuits could help researchers to develop targeted techniques to restore walking, and potentially enable the recovery of more-complex movements," Eiman Azim, a principal investigator at the Salk Institute for Biological Studies in La Jolla, California, and Kee Wui Huang, a postdoctoral fellow in Azim's lab, wrote in a commentary.

Nine people with paralyzing spinal cord injuries participated in the new study. Six were mostly or completely unable to move their legs but retained some feeling in the limbs; the other three participants had no motor control or sensation from the waist down. 

Related: The five (and more) human senses

The nine participants underwent surgery to have electrodes implanted atop their lower spinal cords, below the muscle and bone but outside the membrane that encases the nervous system. Each participant then trained with their implant for five months. They started out by practicing standing, walking and performing various exercises indoors in a weight-bearing harness, and they eventually graduated to training outdoors with a walker for stability. 

These exercises were completed with the EES implant switched on, but in time, four of the nine participants could bear weight and walk with the device switched off, the researchers wrote in their report. 

The team also found that, as each participant regained their ability to walk, the overall activity of their spinal cords decreased in response to the EES — what initially looked like a roaring fire of nerve cell activation dwindled down to a smolder. This hinted that the combination of rehab and electrical stimulation was reorganizing the nervous system, such that fewer and fewer cells were needed to complete the same action. 

"When you think about it, it should not be a surprise because in the brain, when you learn a task, that’s exactly what you see — there are less and less neurons activated" as you improve, co-senior author Grégoire Courtine, a neuroscientist and professor at the Swiss Federal Institute of Technology, Lausanne (EPFL), told Nature.   

The team used rodent-size EES implants to study how this reorganization unfolds in mice with paralyzing spinal cord injuries. The mice completed a course of rehabilitation, similar to the human participants, and throughout, the researchers tracked which of their nerve cells responded to the treatment by changing which genes they had switched on.

This analysis revealed a set of neurons in the lumbar spinal cord that consistently responded to the therapy, even as other neurons became less active. Blocking the activity of these neurons in uninjured mice didn't affect their ability to walk, but in injured mice with paralysis, silencing the cells prevented them from walking again. This suggests that, although other nerve cells might play their own roles in recovery, this particular group is especially important, Courtine told Science.

"The findings are consistent with the idea that certain types of spinal neuron[s] that have lost their inputs from the brain after injury can be 'reawakened' or repurposed to restore movement if they are given the appropriate combination of stimulation and rehabilitation," Azim and Huang wrote. Assuming the findings from the mouse studies carry over to humans, the experiments could lay the groundwork for new-and-improved devices aimed at repairing the spinal cord after injury, they said.

The nerve that enables the human clitoris to detect pleasurable touch contains thousands more nerve fibers than once estimated — about 10,000, rather than 8,000. Medical researchers discovered this by doing something that had never been done before: They actually counted the fibers.

Previously, it was widely accepted that the clitoris contained about 8,000 nerve fibers, but the origins of this number are fuzzy, lead study author Dr. Blair Peters, an assistant professor of surgery in the Oregon Health and Science University (OHSU) School of Medicine, told Live Science.

"The 8,000 number, it wasn't even an actual scientific paper," he said. The number comes from a line in a book called "The Clitoris" (Warren H. Green, Inc., 1976) by physician Dr. Thomas P. Lowry and his then-wife Thea Snyder Lowry, in which the authors briefly mentioned a study of cow clitorises and extended its findings to people. 

"It wasn't based on human data," Dr. Rachel Rubin, an assistant clinical professor of urology at Georgetown University and a urologist and sexual medicine specialist at a private practice in the D.C. area, told Live Science. The cow-derived stat has been cited many times without being fact-checked — until now.

Related: How many organs are in the human body? 

In their research, Peters and their colleagues examined the two dorsal nerves of the clitoris, which are dense bundles of nerve fibers that relay sensory signals from the clitoris to the brain. These nerves run down either side of the clitoral shaft and relay information about touch, pressure and pain, while other nerves handle functions like muscle tone and blood flow.

The sampled dorsal nerves contained between 4,926 and 5,543 nerve fibers each, or an average of 5,140 fibers. With two dorsal nerves per clitoris, that translates to about 10,280 nerve fibers that enable sensation in the pleasure-producing organ. These findings, which have not yet been peer-reviewed, were presented Oct. 27 at a joint scientific meeting of the Sexual Medicine Society of North America and the International Society for Sexual Medicine. 

What's remarkable, Peters said, is that these 10,000 fibers all plug into the clitoral glans, the visible portion of the clitoris located where the labia minora (inner lips) of the vulva meet. In comparison, the median nerve, which runs through the wrist and supplies sensation to most of the hand, contains 18,000 nerve fibers. When you compare the surface area of the clitoral glans to that of the hand, "10,000 compared to that 18,000 becomes shockingly high," he said.

Peters pursued this research, in part, to inform his work as a plastic and reconstructive surgeon specializing in gender-affirming surgeries, including gender-affirming phalloplasty, or the surgical construction of a penis from other tissues in the body. 

To create a penis capable of erogenous sensation, surgeons take tissue from an area of the body with an ample supply of nerves, typically the forearm or thigh, according to the OHSU Transgender Health Program. Once the phallus is made, those nerves are then hooked up to nerves in the pelvis, and ideally, the nerves grow together and begin relaying sensory signals to the brain.    

"I wanted to take a closer look, basically, at the nerves we connect when we make a penis," Peters told Live Science. 

Broadly, research into the basic anatomy of the vulva, which includes the clitoris, could also aid in the diagnosis and treatment of nerve injury and help surgeons navigate procedures near the genitals without causing inadvertent damage.

The new research was made possible by seven transmasculine patients who underwent phalloplasties and volunteered to donate samples of their clitoral tissue. These donated tissues were then preserved, stained blue and magnified 1,000 times under a microscope so that an image-analysis software could count individual nerve fibers.

All the patients underwent testosterone therapy prior to phalloplasty. There is some evidence that testosterone can boost nerve regeneration in the context of an injury, but in normal, healthy nerves, the hormone shouldn't change the number of fibers present, Peters said. "However, this study did not have controls without exposure to testosterone," they said, so it would be worth repeating the study with tissue samples from cisgender women who'd never had testosterone. Such samples would likely come from cadavers, rather than people undergoing surgery.

The new research highlights how little is known about the anatomy and function of the clitoris, Rubin said. This reflects historical biases in medical research that have left modern doctors with huge knowledge gaps. Rubin discussed these historic inequities in a New York Times investigation published in mid-October.     

"It is likely that no doctor has ever examined your clitoris or asked about orgasm in a medical setting," she said. "And that's not because it's not worthwhile."

Editor's note: This story was updated on Nov. 9 to acknowledge a New York Times investigation on the same subject that heavily featured Rubin. The story was originally published on Nov. 1.

Scientists uncovered something unexpected in the fossilized embryo of a worm-like creature from the Cambrian period: the remains of a tiny, doughnut-shaped brain in the primordial animal's head.

The roughly 500 million-year-old fossil is an example of the marine species Markuelia hunanensis, an ancient cousin of penis worms (priapulids) and mud dragons (Kinorhyncha). To date, scientists haven't found fossils of the worm-like weirdos in their adult form, but researchers have uncovered hundreds of pristine embryos that capture different stages of the animals' early development. Each of these embryos measures only about half a millimeter (0.02 inch) across. 

"The thing about Markuelia is, it looks like a mini-adult — it actually looks like a miniature penis worm," which gives scientists an idea of what a mature M. hunanensis likely looked like, Philip Donoghue, a professor of paleobiology at the University of Bristol in England, told Live Science. 

Donoghue and his collaborator Xi-ping Dong, a professor in the School of Earth and Space Sciences at Peking University in Beijing, have examined many of these embryos over the years, but this is the first time they've found one with preserved brain tissue hidden inside. They reported their discovery Oct. 4 in the journal Royal Society Open Science.

Related: Impeccably preserved dinosaur embryo looks as if it 'died yesterday' 

Historically, reports of scientists finding fossilized brain tissue have been controversial because it was once thought that nervous tissue couldn't fossilize, Live Science previously reported. However, in this instance, the evidence looks convincing, said Nicholas Strausfeld, a regents professor in the Department of Neuroscience at the University of Arizona in Tucson who was not involved in the study.

"That seems to me, inescapably, a tissue that is not muscle — and it's not gut either, so what could it be?" Strausfeld told Live Science. "I would say they're neurons," and specifically, brain cells arranged in a ring around what would have once been the animal's gut, he said. 

The exceptional embryo was collected from a fossil deposit known as the Wangcun Lagerstätte in western Hunan, China. There, the teeny-tiny fossil had been encased in a large slab of limestone. Back at their lab at Peking University, Dong and his colleagues carefully dissolved this limestone rock with acid and then manually sorted through the microfossils in the residue.

"You can imagine each one of these [embryos] probably weighs fractions of a gram, but he was literally dissolving down tons, metric tons, of rock," Donoghue said of Dong's efforts to find these embryos over the years. "It's beyond 'needle in a haystack' territory," he said.

Once liberated from the limestone, the embryos were shipped to the Paul Scherrer Institute in Villigen, Switzerland, which houses a particle accelerator measuring about 1,300 feet (400 meters) in diameter. By hurling electrons at approximately the speed of light, the machine generates radiation that can be used for various experiments, Donoghue said. In this case, the team used high-powered X-rays produced by the accelerator to take snapshots of their tiny M. hunanensis embryos. 

"The specimen rotates through 180 degrees within the beam, and it takes 1,501 X-rays as it goes," Donoghue said. These individual X-rays can then be assembled into a detailed 3D model, allowing the team to peer inside each embryo without having to physically smash it open.

"Normally, we don't get preservation of the original anatomy of the organism; we just get the cuticle," meaning the animal's tough outer shell, Donoghue said of the X-rayed embryos. In addition, scientists often see thin lines of mineralization crosshatching the inside of each embryo; such lines are thought to be evidence of microbes that grew over the animal prior to its fossilization. 

Compared with what the team typically observed, the embryo that contained traces of nervous tissue looked starkly different. That embryo bore a clear, organized structure in its head, which the team interpreted to be the animal's ring-shaped brain. What's more, the fossil carried another distinctive structure in its tail, which the team took to be remnants of muscle.     

"In this one specimen, in both the head and the tail, we have this entirely distinct, structured, organized mineralization fabric that's very different to what we see in any other specimen," Donoghue said. "That's why we interpret it's a biological structure that was intrinsic to the original organism, and then it's our job to work out what on Earth it was."

Based on the known relationship of M. hunanensis to animals like penis worms and mud dragons, scientists could reasonably expect its brain to be ring-shaped, so the authors' interpretation of the fossil makes sense, Strausfeld told Live Science. "Setting aside the improbability of [the brain's] fossilization, it would be surprising were it to exhibit a different morphology," the study authors noted in their report.

Notably, this is the first time fossilized nervous tissue has been found in a so-called Orsten-style fossil, the authors added. Such fossils are usually less than 0.08 inch (2 mm) long, are found locked in nodules of limestone and are preserved through a mineralization process whereby the animals' tissue is replaced by calcium phosphate. This process produces a minuscule but highly detailed 3D fossil that typically only preserves the animal's cuticle, not its internal organs. 

"The most interesting thing about our paper is perhaps what it tells us about the potential for future discoveries," Donoghue said. "Nobody had foreseen that you could preserve brains or nervous tissues in calcium phosphate, and maybe it's just a matter of going back and looking for it in museum drawers."

The nervous system is a complex collection of nerves and specialized cells known as neurons that transmit signals between different parts of the body. It is essentially the body's electrical wiring. 

Structurally, the nervous system has two components: the central nervous system and the peripheral nervous system. According to the National Institutes of Health, the central nervous system is made up of the brain, spinal cord and nerves. The peripheral nervous system consists of sensory neurons, ganglia (clusters of neurons) and nerves that connect to one another and to the central nervous system.

Functionally, the nervous system has two main subdivisions: the somatic, or voluntary, component; and the autonomic, or involuntary, component. The autonomic nervous system regulates certain body processes, such as blood pressure and the rate of breathing, that work without conscious effort, according to Merck Manuals. The somatic system consists of nerves that connect the brain and spinal cord with muscles and sensory receptors in the skin.

What is the nervous system?

Nerves are cylindrical bundles of fibers that start at the brain and central cord and branch out to every other part of the body, according to the University of Michigan Medical School. 

Neurons send signals to other cells through thin fibers called axons, which cause chemicals known as neurotransmitters to be released at junctions called synapses, the NIH noted. There are over 100 trillion neural connections in the average human brain, though the number and location can vary. For example, a study published in the journal Proceedings of the National Academy of Sciences (PNAS) found that out of the 160 participants studied, the brains of highly creative people have more connections among three specific regions of the brain than less creative thinkers.

"You have these three different systems that are all located in different parts of the brain, but they are all co-activated at once," said lead study author Roger Beaty, a postdoctoral fellow studying cognitive neuroscience at Harvard University. "People who are better able to co-activate them [came] up with more-creative responses."

A synapse gives a command to the cell and the entire communication process typically takes only a fraction of a millisecond. Signals travel along an alpha motor neuron in the spinal cord 268 mph (431 km/h); the fastest transmission in the human body, according to Discover magazine.

Sensory neurons react to physical stimuli such as light, sound and touch and send feedback to the central nervous system about the body's surrounding environment, according to the American Psychological Association. 

Motor neurons, located in the central nervous system or in peripheral ganglia, transmit signals to activate the muscles or glands. Glial cells, derived from the Greek word for "glue," are specialized cells that support, protect or nourish nerve cells, according to the Oregon Institute of Health and Science University. 

The brain's connections and thinking ability grew over thousands of years of evolution. For example, a virus bound its genetic code to the genome of four-limbed animals, and the code can still be found in humans' brains today, according to two papers published in the January 2018 journal Cell. This code packages up genetic information and sends it from nerve cells to other nearby nerve cells, a very important process in the brain. 

Divisions of the nervous system

When we think of the nervous system, our thoughts immediately go to the brain. The brain is a hive of neuronal activity, with billions of interwoven neurons firing to preserve and recall memories, coordinate thoughts and speech, and plan future actions. Along with the spinal cord, the bone-clad parts of our nervous system are naturally called the central nervous system.

The majority of our neurons are shielded behind protective fluid and bone, where they receive signals from and dictate to organs around the body. However, the signals sent from the central nervous system must have some means of reaching their target organs. And for that they need to connect to nerves that stretch from the central nervous system all the way to the extremities of the body. This second network of nerves is called the peripheral nervous system. Together, the central and peripheral form the major divisions of the nervous system, according to the National Cancer Institute.

The peripheral nervous system is responsible for many functions, and as such has numerous sub-divisions that specialise on different tasks. The sensory, or afferent, division receives signals from the periphery and carries these into the central nervous system. The motor, or efferent, division transmits signals for actions outward from the central nervous system to the peripheral organs and muscles. These motor functions come in two forms: somatic, and autonomic. Somatic functions are perhaps the easiest concept of the nervous system to grasp, as these dictate all our voluntary actions, such as choosing to pick up a cup, or jump on the bed, according to the medical library LibreTexts. 

Not all somatic motor functions are voluntary, however. Some are automatic, pre-programmed responses built into our bodies that help us cope with danger, known as somatic reflexes. You’ll notice such a reflex when you accidentally touch a hot stove, step on a sharp object, or something flies toward your eye - your body reacts before you’re aware of it. Your hand pulls away, you hop onto the other foot, your eyelid slams shut. This is all the work of somatic reflexes, which can act incredibly quickly as they do not require voluntary input from the brain. Such reflexes can come in different flavours; pulling your hand away from danger is known as a flexor or withdrawal reflex, whereas stepping on a sharp object initiates a crossed-extensor reflex. This latter reflex automatically triggers multiple motor functions, as one leg retracts the other leg simultaneously expands and becomes more stable, preventing us from falling over.

The innate, hard-wired reflex responses of our peripheral nervous system help keep us safe from danger, but they are not the only automatic functions performed by the peripheral nervous system. When actions are not voluntary, or somatic, they are autonomic, which means they operate independently of conscious thought. Such processes include the heart beat, the churning of food in the digestive tract by contracting muscles, and respiration. While our brain can assume control of a few of these processes (think of holding your breath), autonomic functions will continue to operate even when we fall asleep or if we are knocked unconscious. 

The processes that we cannot control, however, are by no means unchanging. Instead the organs under the control of the autonomic nervous system are regulated by a balance between the sympathetic and parasympathetic nervous systems. Depending on the stimulus, these systems increase or decrease activity of our internal organs, helping to ensure our body is always ready to respond to the challenge at hand.

Nervous system disorders

"Of all the diseases of the nervous system, the most common difficulty that people have is pain, and much of that is nerve-related," according to Dr. Shai Gozani, founder and CEO of NeuroMetrix, a medical device company. "There are 100 million people who live with chronic pain."

Parkinson’s disease

The basal ganglia are found deep within the brain, in an area responsible for controlling movement. These nerves produce a compound known as dopamine, which is important in coordinating numerous functions including executive functions and motor control. Although the cause is not yet clear, sometimes the basal ganglia can become impaired and begin to die. The result of this is Parkinson’s disease, as the loss of dopamine gradually hampers key functions such as walking, talking, and memory recall. These effects are compounded by the loss of nerves responsible for producing norepinephrine, a key compound in the sympathetic nervous system needed to regulate heart rate and blood pressure. Medicines that increase the amount of dopamine in the brain can help combat symptoms of the disease, according to the National Institute of Aging.

Bell’s Palsy

Major nerves spread outward from the central nervous system to various organs and tissues, with each powering specific functions. Cranial nerve VII is known as the facial nerve, as it controls many of the muscles on our face including blinking and smiling. When this nerve is inflamed, damaged, or otherwise disrupted Bell’s palsy can occur, which involves the facial muscles becoming weakened or paralysed, according to the National Institute of Neurological Disorders and Stroke. This typically affects only one side of the face, causing symptoms such as drooping of the mouth on one side and a loss of control of an eyelid, giving the affected side a slack appearance. The full symptoms of Bell’s palsy are often temporary, with some or total recovery of the affected areas occurring with six months. While it is not always clear what causes the cranial nerve to swell and Bell’s palsy to occur, scientists believe that a recurring viral infection of the nervous system elicits an immune response that triggers the nerve damage.

Multiple sclerosis

Neurons are the agents of signalling in our bodies, but they do not work alone. Axons, which carry signals away from the neuron’s cell body, are coated in a sheaf of myelin. Myelin sheaves are produced in the central nervous system by cells called oligodendrocytes, enabling myelin’s function of protecting and facilitating nerve conductivity, according to the National Multiple Sclerosis Society. In multiple sclerosis, an abnormal immune response within the central nervous system strips away the protective myelin and causes lots of nerve scarring (sclerosis), which gives the disease its name. Research efforts are underway to treat the disease by encouraging myelin regeneration.

Peripheral neuropathy

While several degenerative nervous system disorders primarily or exclusively impact the central nervous system, there are a collection of diseases that instead impact the peripheral nervous system. Together these diseases are referred to as peripheral neuropathies. As the impacted region is the peripheral nervous system, such neuropathies lead to loss of sensation and regulatory control of extremities. These include a loss of coordination and feeling in fingers and toes, and a lack of balance, according to the University of Michigan Health. The causes of peripheral neuropathy are yet to be fully elucidated, but scientists have determined diabetes, which causes protracted periods of high blood sugar, as one of the primary causes. 

Diagnosing nervous system conditions

There are a number of tests and procedures to diagnose conditions involving the nervous system. In addition to the traditional X-ray, a specialized X-ray called a fluoroscopy examines the body in motion, such as blood flowing through arteries, according to the NIH. 

Other standard neurological exams include an MRI (magnetic resonance imaging), CT scan, and an electroencephalogram (EEG), which records the brain's continuous electrical activity. Positron emission tomography (PET) is a procedure that measures cell or tissue metabolism and brain activity to detect tumors or diseased tissue or tumors, the NIH noted.

A spinal tap places a needle into the spinal canal to drain a small amount of cerebral spinal fluid that is tested for infection or other abnormalities, according to the NIH.

Neurology: Study of the nervous system

The branch of medicine that studies and treats the nervous system is called neurology, and doctors who practice in this field of medicine are called neurologists. Once they have completed medical training, neurologists complete additional training for their specialty and are certified by the American Board of Psychiatry and Neurology (ABPN).

There are also physiatrists, who are physicians who work to rehabilitate patients who have experienced disease or injury to their nervous systems that impact their ability to function, according to the ABPN.

Neurosurgeons perform surgeries involving the nervous system and are certified by the American Association of Neurological Surgeons.

Additional resources

For more information about your body's nervous system, check out “The Human Nervous System” by Juergen K. Mai and “The Big Book Of The Human Body” by Katherine Marsh

Bibliography

• James Ashley, et al, “Retrovirus-like Gag Protein Arc1 Binds RNA and Traffics across Synaptic Boutons”, Cell, Volume 172, January 2018. 
• Roger E. Beaty, “Robust prediction of individual creative ability from brain functional connectivity”, PNAS, Volume 115, January 2018. 
• Valerie Ross, “Numbers: The Nervous System, From 268-MPH Signals to Trillions of Synapses”, Discover Magazine, mAY 2011. 
• University of Michigan Health, “Peripheral Neuropathy”, August 2020. 
• National Institute of Neurological Disorders and Stroke, “ Bell's Palsy Fact Sheet”, November 2021.  
• National Institute of Aging, “Parkinson’s Disease”, May 2017. 
• National Library of medicine, “Neurologic Diseases”, March 2022. 
• National Multiple Sclerosis Society, “What is Myelin”, accessed March 2022. 

Ebola can lurk in fluid-filled cavities in the brain and kill monkeys, even after the animals have been treated for the disease and seem to have recovered, a new study shows.

The study, conducted in rhesus macaques (Macaca mulatta), hints at why some human Ebola survivors relapse and die months or years after recovering from their initial infections, The Scientist reported. Past studies of monkeys and humans suggested that the Ebola virus can lurk in various places in the body — including the testes, eyes and brain — and the new report may reveal where in the brain the virus persists.

The research, published Wednesday (Feb. 9) in the journal Science Translational Medicine, included 36 rhesus macaques that scientists infected with Ebola. The team treated the monkeys with monoclonal antibodies, which latch onto the virus and interfere with its ability to infect cells; all of the treatments used for the study have been approved for use in humans. After the treatment, the team screened the monkeys' blood for Ebola virus genetic material, or RNA, and also searched for viral RNA in the primates' cerebrospinal fluid (CSF), the clear fluid that surrounds the brain and spinal cord.

Related: The deadliest viruses in history 

The researchers found that, two and four weeks after the monkeys' initial Ebola exposures, seven of the monkeys carried high levels of Ebola RNA in their CSF, hinting that the animals had developed persistent infections in their nervous systems. Two of these seven monkeys then fell ill, despite having recovered from their initial infections. These two macaques died 30 and 39 days after their initial exposure to the virus, while most of the other monkeys in the study survived for months.

The surviving macaques were euthanized about four months after infection so that the team could examine the monkeys' brain tissue and compare it to that of the monkeys that died from Ebola. In the seven macaques with viral RNA in their CSF, the researchers discovered Ebola RNA in the brain ventricles, the cavities in the brain where CSF is produced. 

And in the two monkeys that died, the team observed "massive tissue damage and inflammation" throughout this ventricular system, but the animals' other organs appeared completely normal, lead study author Xiankun Zeng, a researcher at the U.S. Army Medical Research Institute of Infectious Diseases, told The Scientist.

The presence of Ebola RNA in the CSF has been linked to at least one case in which a person's infection relapsed following their initial recovery, according to a 2021 report published in The New England Journal of Medicine. Because of this, Zeng told The Scientist that he suspects that the virus may hide in the ventricles of humans just as his team observed in macaques. 

In the future, improved Ebola treatments could include a combination of monoclonal antibodies and powerful antivirals that can flush the virus from these brain regions, as well as the eyes and testes. This would reduce the risk of relapse, Zeng said.   

There is an "urgent need" to test and refine such treatments in animal models, Miles Carroll, an emerging-viruses researcher at the University of Oxford who was not involved in the study, told The Scientist. And in order to prevent Ebola outbreaks, it's especially important to clear persistent Ebola from the testes, as research suggests that the most likely route of tranmission from a relapsing Ebola survior to another person would be sexual transmission, mediated by infected semen, he said. (In general, Ebola spreads when blood, secretions or other body fluids containing the virus come into contact with broken skin or the mucous membranes of a healthy individual.)

"In the absence of such therapies, [Ebola virus disease] survivors may continue to be a potential source of future human-to-human transmission," he told The Scientist.

Read more about the new study in The Scientist.

Originally published on Live Science.

When faced with imminent physical danger, the human body’s sympathetic nervous system triggers our "fight-or-flight" response. The sympathetic nervous system is a normally harmonized network of brain structures, nerves and hormones that, if thrown off balance, can result in serious complications.

What is a sympathetic nervous system?

The sympathetic nervous system makes up part of the autonomic nervous system, also known as the involuntary nervous system. Without conscious direction, the autonomic nervous system regulates important bodily functions such as heart rate, blood pressure, pupil dilation, body temperature, sweating and digestion, according to a review in the American Journal of Pharmaceutical Education. Research suggests that distinct types of nerve cells, called neurons, control these different physical reactions by directing the action of skeletal muscle, cardiac muscle and gland secretion. The system allows animals to make quick internal adjustments and react without having to think about it.

The sympathetic nervous system directs the body's rapid involuntary response to dangerous or stressful situations. A flash flood of hormones boosts the body's alertness and heart rate, sending extra blood to the muscles. Breathing quickens, delivering fresh oxygen to the brain, and an infusion of glucose is shot into the bloodstream for a quick energy boost. This response occurs so quickly that people often don't realize it's taken place, according to Harvard Medical School. For instance, a person may jump from the path of a falling tree before they fully register that it's toppling toward them.

The sympathetic nervous system doesn't destress the body once the tree is felled or the danger has passed. Another component of the autonomic nervous system, the parasympathetic nervous system, works to calm the body down, according to the Clinical Anatomy of the Cranial Nerves, published in 2014 by Academic Press. To counter the fight-or-flight response, this system encourages the body to "rest and digest." Blood pressure, breathing rate and hormone flow return to normal levels as the body settles into homeostasis, or equilibrium, once more.

The sympathetic and parasympathetic nervous systems work together to maintain this baseline and normal body function.

How is the sympathetic nervous system organized?

Structures in the brain, spinal cord and peripheral nervous system support the function of the sympathetic nervous system, according to a 2016 review in the journal BJA Education. Receptors in internal organs of the chest and abdomen collect information from the body and send it up to the brain through the spinal cord and cranial nerves. The hypothalamus, a brain structure important for regulating homeostasis, receives signals from the body and tunes the activity of the autonomic nervous system in response.

This brain structure also gathers information from areas higher in the brain, such as the amygdala, according to a review in the journal Biological Psychiatry. Often called the emotional brain, the amygdala pings the hypothalamus in times of stress.

The hypothalamus then relays the alert to the sympathetic nervous system and the signal continues on to the adrenal glands, which then produce epinephrine, better known as adrenaline. This hormone triggers the profuse sweating, rapid heartbeat and short breaths we associate with stress. If the danger persists, the hypothalamus sends a new message through the nerve system grapevine, instructing the adrenal glands to produce the hormone cortisol to keep the stress response rolling.

Outgoing commands from the sympathetic nervous system exit the spinal cord in the thoracolumbar region, or the mid to lower spine. Sympathetic neurons exit the spinal cord and extend in two columns on either side of it. These neurons then tag a second set of nerve cells into the relay, signaling them with help from the chemical messenger acetylcholine.

Having picked up the baton, the second set of neurons extends to smooth muscles that execute involuntary muscle movements, cardiac muscles and glands across the body. Often, the parasympathetic nervous system communicates with the same organs as the sympathetic nervous system to keep the activity of those organs in check.

What happens when it doesn't work?

The sympathetic and parasympathetic nervous systems rest on either side of a wobbling scale; each system remains active in the body and helps counteract the actions of the other. If the opposing forces are mostly balanced, the body achieves homeostasis and operations chug along as usual. But diseases can disrupt the balance.

The sympathetic nervous system becomes overactive in a number of diseases, according to a review in the journal Autonomic Neuroscience. These include cardiovascular diseases like ischemic heart disease, chronic heart failure and hypertension. A boost of sympathetic signaling raises the blood pressure and enhances tone in smooth muscles, which may cause hypertension.

Beyond cardiovascular ailments, sympathetic dysfunction has been associated with kidney disease, type II diabetes, obesity, metabolic syndrome and even Parkinson's disease.

"Everyone thinks about Parkinson's disease in terms of its motor symptoms, but these autonomic symptoms actually appear long before," said Dr. Marina Emborg, director of the Preclinical Parkinson's Research Program at the University of Wisconsin-Madison. Changes in sympathetic nervous activity are evident in the skin, pupils and especially the heart.

"Some patients [with Parkinson's] describe that they are more tired or have fatigue, but really, problems in the heart contribute to these overall symptoms," Emborg told Live Science.

Parkinson's damages the sympathetic neurons that help maintain levels of epinephrine and norepinephrine in the body — chemicals that tell the heart when to pump harder, such as when you move to stand up or exercise. Damage to these neurons can result in a lack of blood flow in patients with Parkinson's, so they often feel lightheaded upon standing, which dramatically increases their risk of falls.

Sympathetic dysfunction also underlies mental health conditions such as anxiety, depression and chronic stress, an article in Forbes reported. In short bursts, the body's physical stress response can be useful and grant an energizing boost of mental focus. If prolonged, however, the stress signals whizzing through the body wreak havoc. Besides maintaining a mental feeling of constant stress, the extra epinephrine and cortisol damage blood vessels, increase blood pressure and promote a buildup of fat.

So, while the fight-or-flight response serves a purpose, you don't want it switched on all the time.

Additional resources

Read more about the body's response to stress at this page from the National Institute of Mental Health. To find more information about autonomic disorders from the Cleveland Clinic. For more information on the brain, check out "The Human Brain Book: An Illustrated Guide to its Structure, Function, and Disorders" by Rita Carter or "Brains Explained: How They Work & Why They Work That Way" by Alison Caldwell. 

Bibliography

Grassi Guido et al, “The Sympathetic Nervous System Alterations in Human Hypertension”, Circulation Research, Volume 116, March 2013, https://doi.org/10.1161/CIRCRESAHA.116.303604. 

M. Sinski et al, “Why Study Sympathetic Nervous System”, Journal OD physiology and Pharmacology, Volume 11, 2006. 

Tanja Schlereth & Frank Birklein, “The Sympathetic Nervous System and Pain”, NeroMolecular medicine, Volume 10, November 2007, https://doi.org/10.1007/s12017-007-8018-6. 

Gino Seravelle et al, “Sympathetic Nervous System, Sleep, and Hypertension”, Current Hpertension Reports, Volume 20, July 2018, https://doi.org/10.1007/s11906-018-0874-y. 

Two tiny fossils, each smaller than an aspirin pill, contain fossilized nerve tissue from 508 million years ago. The bug-like Cambrian creatures could help scientists piece together the evolutionary history of modern-day spiders and scorpions.

Still, it's not clear exactly where these fossils — both specimens of the species Mollisonia symmetrica — fit on the arthropod evolutionary tree, said Nicholas Strausfeld, a regents professor in the Department of Neuroscience at the University of Arizona, who was not involved in the study. 

That's because some features, like the animals' eyes and nerve cords, can be clearly identified in the fossils, but other parts of the nervous system cannot be so easily spotted. In particular, it's unclear whether or not the animals carry a brain-like bundle of nerves called a synganglion, and without this key piece of evidence, their relation to other animals remains fuzzy, Strausfeld said.

Related: From dino brains to thought control — 10 fascinating brain findings

Where the synganglion would sit, instead there's "this mess in the middle of the head," said first author Javier Ortega-Hernández, an invertebrate paleobiologist at Harvard University and curator of the Harvard Museum of Comparative Zoology. The researchers can tell that this mess is nerve tissue, but they can't discern its exact organization. 

"It is … true that we do not have every single characteristic of the nervous system of this animal mapped out, because the fossils only tell us so much," Ortega-Hernández said. The researchers acknowledge this uncertainty in their new report, published Jan. 20 in the journal Nature Communications, and present a few different ideas as to how these fossils relate to ancient and modern-day critters. If more fossilized M. symmetrica are uncovered in the future, the species' place on the tree of life may eventually be resolved.  

'A stroke of luck' 

Finding fossilized nerve tissue from the Cambrian period, which took place between about 543 million and 490 million years ago, is a "rarity," Ortega-Hernández said. "It's really a stroke of luck."

Scientists uncovered the first evidence of a fossilized arthropod brain from the Cambrian period about a decade ago, according to a 2012 report in the journal Nature Communications; arthropods are invertebrate animals in the phylum Arthropoda, a group that includes modern insects, crustaceans and arachnids, like spiders. Since that initial discovery 10 years ago, preserved nerve tissue has been found in more than a dozen Cambrian fossils, most of them arthropods, Ortega-Hernández said.

The fossils featured in the new study were found not at a field site, but in the depths of the museum collections at the Harvard University Museum of Comparative Zoology in Cambridge, Massachusetts, and the Smithsonian Institution in Washington, D.C. Both specimens were discovered in mid-Cambrian Burgess Shale deposits from British Columbia.

The Harvard fossil measures about 0.5 inches (13 millimeters) long and 0.1 inches (3.5 mm) wide at its widest point; the fossil is oriented such that you're looking down at the arthropod from above. The Smithsonian fossil, on the other hand, offers a side-view of M. symmetrica; this specimen measures only 0.3 inches (7.5 mm) long and 0.06 inches (1.7 mm) tall. 

Related: Ancient footprints to tiny 'vampires': 8 rare and unusual fossils 

To the naked eye, neither fossil looks particularly exciting, Ortega-Hernández said. Regarding the miniscule Smithsonian fossil, in particular, "superficially, it is extremely unremarkable," he said. M. symmetrica has a simple exoskeleton, consisting of a head shield, segmented trunk and posterior shield — somewhat like the exoskeleton of a pillbug, but long and skinny. 

The researchers suspect that the arthropod also had seven pairs of tiny appendages, two fangs and six pairs of little limbs; that's based on a 2019 study, published in the journal Nature, that described a fossil from a different species in the Mollisonia genus that bore such appendages. However, it's highly unusual to find Mollisonia fossils with intact limbs, and both fossils used in the new study lack appendages, Ortega-Hernández noted.

Despite the fossils' lack-luster appearance, when he placed the Smithsonian M. symmetrica fossil under a microscope, he spotted something intriguing, Ortega-Hernández said. "I realized, 'Ooh, there's something funky inside of this animal, inside of this fossil,'" he said. He found that locked inside both of these inconspicuous arthropods were well-preserved nervous systems. The fossilized nerves look like inky black splotches, because the fossilization process transformed the tissue into organic carbon films. 

In the Smithsonian fossil, a bulbous eye can be seen in the arthropod's head and a nerve cord can be clearly seen running down the length of its belly, with some nerves jutting out from its underside. In the Harvard specimen, one can see two huge, orb-like eyes on the head, and a bit of the nerve cord peeking out from beneath the animal's digestive tract, which obscures the rest of the cord. 

In both fossils, the study authors reported seeing optic nerves that run from the arthropods' eyes into the main body, but Strausfeld said the evidence for these nerves is "ambiguous," and ideally, these features would be clearer. And in both specimens, the authors noted that there's some sort of nerve tissue present in the head, but it's unclear whether this structure is a brain-like synganglion or something else entirely.

"We can see there's something in there, but we don't have enough resolution to be able to say, 'Oh, it's definitely organized in this way or that way,'" Ortega-Hernández said.

Uncertainty in the data 

This uncertainty in the fossil record means the precise relationship of M. symmetrica to other animals also remains murky, Ortega-Hernández said. But based on the features present in the arthropods, the team constructed two evolutionary trees. 

Both trees indicate that M. symmetrica and modern chelicerates share a common ancestor, suggesting that the ancient animal's relatively simple nervous system gave rise to the highly condensed brain seen in modern-day members of this group, such as scorpions, spiders, horseshoe crabs and ticks. However, the trees differ in where they position other important arthropod groups from the Cambrian, including one known as the megacheirans; these groups have similar nervous systems to modern chelicerates. 

Depending on where these various groups sit on their evolutionary tree, their placement either shows that chelicerate-like brains evolved in a stepwise manner through time, or it hints that such nervous systems evolved independently and at different times in some Cambrian arthropods and modern chelicerates, through convergent evolution, Ortega-Hernández said.

With the data at hand, Strausfeld said he would be "cautious" about attempting to place M. symmetrica anywhere on an evolutionary tree. In order to do so, he said he'd need clearer evidence of how the arthropods' optic nerves and synganglion (or lack thereof) are structured, as well as evidence of nerves extending out to the roots of the animal's limbs. 

"I think one needs a better preparation, a better specimen" than the ones examined so far, Strausfeld said. "Maybe there's another specimen lying around somewhere in a museum."

Originally published on Live Science. 

The human body is a complex network of systems that work together to keep life-sustaining processes running smoothly. These systems break down food for fuel, clear away waste, repair damaged tissues and DNA, fight infectious germs and monitor the outside world so we can move through it safely. 

Many scientists spend their days working to understand how each bodily system performs its jobs, how the systems interact, and what can happen when one or more of them falter. Such malfunctions can stem from aging or disease, for instance, and through medical care, doctors aim to get derailed systems back on track. 

Here's a quick rundown of the systems of the human body, its vital organs and its "vestigial" organs, as well as a few fascinating facts about how the body works.

What are the different systems of the human body? 

Our bodies consist of a number of biological systems that carry out specific functions necessary for everyday living. Some organs and tissues play roles in multiple systems at once.

Related: Strange, two-faced brain cells confirmed to exist, and they may play a role in schizophrenia 

Circulatory: The job of the circulatory system is to move blood, nutrients, oxygen, carbon dioxide and hormones around the body. It consists of the heart, blood, blood vessels, arteries and veins. According to the Cleveland Clinic, the adult human body's network of blood vessels is more than 60,000 miles (around 100,000 kilometers) long. 

Digestive: The digestive system consists of a series of connected organs that together allow the body to break down and absorb nutrients from food and remove waste. It includes the mouth, esophagus, stomach, small intestine, large intestine, rectum and anus. The large intestine is home to microorganisms that are collectively called the gut microbiome and influence our health in various ways. The liver and pancreas also have roles in the digestive system because they produce digestive juices filled with enzymes to break down the components of food, such as carbohydrates, fats and proteins, according to the National Institute of Diabetes and Digestive and Kidney Diseases.

Endocrine: The endocrine system consists of a network of glands that secrete hormones — long-range chemical messengers that regulate how cells and tissue function — into the blood. These hormones, in turn, travel to different tissues and regulate many bodily functions, such as metabolism, growth and sexual function, according to Johns Hopkins Medicine. For example, the pancreas releases the hormones insulin and glucagon to regulate blood sugar. Conditions like diabetes and insulin resistance arise from the body having too little insulin or not responding to it adequately. 

Related: Meet the 'exclusome': A mini-organ just discovered in cells that defends the genome from attack

Immune: The immune system is the body's defense against bacteria, viruses and other pathogens that may be harmful. Components of the system include the lymph nodes, which contain infection-fighting cells called lymphocytes. These lymphocytes are one of many types of leukocyte, or white blood cell. The immune system also includes the spleen, the bone marrow and a gland called the thymus. The immune system can learn to recognize antigens — proteins on the surface of bacteria, fungi and viruses — and alert the body to their presence. Some immune cells make proteins called antibodies that attach to these antigens and mark invaders for destruction. 

Lymphatic: The lymphatic system includes the lymph nodes, lymph ducts and lymph vessels and is considered part of the immune system. Its main job is to make and move lymph, a clear fluid that contains white blood cells. The lymphatic system also removes excess lymph fluid from the body's tissues and returns it to the blood.

Nervous: The nervous system controls both voluntary actions, such as conscious movements, and involuntary actions,like breathing, and it sends signals to and detects signals from different parts of the body. Conscious actions are controlled by the somatic nervous system, while involuntary actions are controlled by the autonomic nervous system. The autonomic nervous system dictates whether we're in "rest and digest" or "fight or flight" mode. The nervous system can further be split up into the central nervous system (CNS), which includes the brain and spinal cord, and the peripheral nervous system, or the nerves connecting the CNS to every other part of the body.

Muscular: The body's muscular system consists of hundreds of muscles that aid movement, blood flow and other bodily functions, according to the Library of Congress. There are three types of muscle: skeletal, which is connected to bone and helps with voluntary movement; smooth, which is found inside organs and helps to move substances through them; and cardiac, which is found in the heart. The body's largest muscle by mass is the gluteus maximus, but the two latissimus dorsi are the largest in terms of surface area.

Related: Why is it harder for some people to build muscle than others?

Reproductive: The reproductive system allows humans to produce offspring. The male reproductive system includes the penis and the testes, which produce sperm. The female reproductive system includes the vagina, uterus and ovaries, which produce eggs. During fertilization, a sperm cell will fuse with an egg cell that, in a successful pregnancy, will then implant in the uterus. The fertilized egg will then mature into what's called a blastocyst, then an embryo and, finally, a fetus. A placenta forms to support this process. 

Skeletal: Our bodies are supported by the skeletal system, which contains between 206 and 213 bones in an adult human body, due to slight variations in people's anatomy, according to the medical resource StatPearls. These bones are connected by tissues called tendons, ligaments and cartilage. As infants, humans have about 300 bones, but some fuse together as the child grows. The skeleton not only helps us move but is  also involved in the production of blood cells and the storage of calcium. The teeth are also part of the skeletal system, but they aren't considered bones. The smallest bones in the body are found in the ear, and the largest is the femur, or thigh bone, which is also one of the heaviest body parts.

Respiratory: The respiratory system allows us to take in oxygen and expel carbon dioxide through breathing. It includes the lungs; trachea, or windpipe; and the diaphragm, a muscle that pulls air into and pushes air out of the lungs.

Urinary: The urinary system helps eliminate a waste product called urea, which is produced when certain foods are broken down. The system includes the two kidneys; two ureters, or tubes leaving the kidneys; the bladder; two sphincter muscles; and the urethra. The kidneys filter blood in the body to make urine that then travels down the ureters to the bladder and exits the body through the urethra.

Integumentary: The skin, hair and nails make up the integumentary system. Skin is the body's largest organ. It protects our innards from the outside world, serving as our first defense against bacteria, viruses and other pathogens, for instance. Our skin also helps regulate body temperature and eliminate waste through perspiration, or sweat. 

Related: Scientists discover new way humans feel touch 

What are the body's vital organs?

Click the purple circles to learn about the body's vital organs, including the brain, lungs, heart, liver and kidneys. They're considered vital because you need a functioning brain, heart, liver, at least one kidney and at least one lung to survive. That said, there are medical devices and treatments that can make up for a loss of function in these organs, at least temporarily — for example, ECMO machines can do the work of the heart and lungs, and dialysis can filter the blood of people with kidney failure.

Fast facts

• The average adult male body contains about 36 trillion cells, the average adult female body contains 28 trillion cells and a 10-year-old has about 17 trillion. 
• It's often said that there are 78 organs in the human body, but the number actually differs depending on whom you ask. 
• There's a popular idea that the body replaces itself every seven years. But that's not really true, because tissues renew themselves at different rates. 
• Oxygen is the most common element in the human body, followed by carbon. 
• The average adult body contains about 1.2 to 1.5 gallons (4.5 to 5.5 liters) of blood. 
• Humans' average body temperature has fallen slightly over time, so it's no longer 98.6 degrees Fahrenheit (37 degrees Celsius). 
• The most detailed map of the human brain to date contains more than 3,300 types of brain cells. 

What are vestigial organs?

There are arguably some parts of the human body that don't serve any useful purpose, such as the male nipple. That said, the usefulness of some organs is still up for debate, as scientists have often judged the worth of body parts before discovering their purposes. 

Broadly speaking, vestigial body parts are defined as those that have lost their original physiological significance to humans over the course of evolutionary history. The idea is that, while we inherited them from an ancient ancestor, we could really do without them in the modern day. 

Wisdom teeth are held up as one example of a vestigial body part, as the modern human jaw is often too small to accommodate a third set of molars. Some people also carry remnants of a vomeronasal organ that is largely thought to be nonfunctional in humans; animals use equivalent organs to detect each other's pheromones. 

Some scientists consider the human tailbone, or coccyx, vestigial because it's no longer a full-blown tail. But it's far from useless, as it still anchors many muscles, ligaments and tendons. And the appendix has gotten a bad rap for supposedly being both vestigial and useless, but more recently, scientists have uncovered possible functions for the long-maligned body part. 

Ever wonder why some people build muscle more easily than others or why freckles come out in the sun? Send us your questions about how the human body works to community@livescience.com with the subject line "Health Desk Q," and you may see your question answered on the website!

Editor's note: This page was last updated on April 5, 2024.

Jellyfish may be brainless, yet they can do surprisingly complex things with their simplistic nervous systems. Now, by fiddling with the genes of jellyfish, researchers have devised a way to spy on the animals' inner workings. 

In the new study, the researchers created a model using the jellyfish species Clytia hemisphaerica, a transparent, umbrella-shaped jellyfish with a tube-like mouth at its center. The teeny jellyfish grows to be only 0.4 inches (1 centimeter) in diameter, meaning the team could place the whole jellyfish under the microscope and observe its entire nervous system at once.

While the human brain serves as a centralized control center for the body, jellyfish have no such structure in their nervous systems. Instead, many jellyfish carry a diffuse "net" of nerves that radiates symmetrically from the center of their bodies; in addition, they have a nerve ring that runs around the bottom of the bell — the half-moon-shaped portion of the jellyfish. Some jellyfish lack nerve nets and have only nerve rings, according to a 2013 report in the journal Current Biology, but C. hemisphaerica has both of these structures. 

The big question is, with no centralized control over their movements, how do these teensy jellyfish perform coordinated behaviors? For instance, how do the blobby critters snatch shrimp from the water column and then fold in half to pull the snacks toward their tubular mouths?

Related: From dino brains to thought control — 10 fascinating brain findings 

To answer this question, the team raised a batch of C. hemisphaerica with a genetic modification that coded for a protein called GCaMP, which glows green when it comes into contact with calcium. 

The special glowing protein was inserted into a location in the jellyfish genome so that it only lit up in active neurons, said first author Brandon Weissbourd, a postdoctoral scholar in biology and biological engineering at the California Institute of Technology. "When neurons are active, the amount of calcium [inside the neurons] goes up, so GCaMP becomes more fluorescent. This means that neural activity looks like flashing," Weissbourd told Live Science in an email. 

But jellyfish are naturally luminescent. So to see their engineered flashing more clearly, the team used CRISPR to snip out a specific gene that makes a different fluorescent protein, one that kept outshining the GCaMP they had inserted, he said.

With their jellyfish thus transformed into miniature light shows, the team ran a number of experiments to see which neurons lit up during their typical feeding behaviors. They found that, when the jellyfish latched onto a brine shrimp, or came into contact with a "shrimp extract" made by the team, a group of neurons physically near the shrimp suddenly lit up. 

Related: Weird animal facts

This activation didn't ripple through the entire jellyfish, like how a stone plopped in a puddle would send ripples across its entire surface. Rather, only neurons within a well-defined, wedge-shaped region of the bell lit up in response to the shrimpy snack. This wedge of active neurons was shaped like  like a single pizza slice within a circular pie, according to a statement. The neurons that were closest to the shrimp lit up first, the team found, and then a slew of strobe lights would illuminate the rest of the slice.

So for example, if a shrimp was placed at the far edge of the pizza slice, onto its "crust," the crust would light up first, followed by the rest of the slice. This ripple effect coincided with the jellyfish folding up in the corner of its bell, in order to bring the shrimp to its mouth. 

The team didn't expect to observe this level of organization within the seemingly unstructured nerve net, Weissbourd said. "The finding of an intrinsic structure within the network was certainly surprising," he said. 

Looking forward, the team plans to investigate how jellyfish exert control over all their behaviors, not just feeding, and they plan to study different species of jellyfish, which perform different behaviors to C. hemisphaerica, Weissbourd said. For instance, while some jellyfish perform a similar food-passing behavior as C. hemisphaerica, others instead use long-reaching mouthparts to pluck food from their tentacles. "Given the diversity of jellyfish, and that so many of them are small and transparent, I think they could provide an exciting platform in the future for understanding how nervous systems evolve."

These studies of strobing jellyfish could also shed light on basic principles that govern all nervous systems, from the most simplistic to the most complex. "The idea is to develop experimental and theoretical approaches towards understanding how simpler nervous systems work as a step towards understanding the human brain, which is orders of magnitude more complex," Weissbourd told Live Science.

The team published their findings Nov. 24 in the journal Cell. 

Originally published on Live Science.

Imagine you're driving down the highway, enjoying the start of a long road trip, when all of a sudden one of the children in your back seat moans, "I don't feel so good." Your immediate response, besides scrambling for a barf bag, would probably be to crack the windows to let in fresh air.

So why does cold air help get rid of nausea? 

"When trying to understand why fresh, circulating, or cold air seems to help alleviate symptoms of nausea, it's ideal to look at research related to motion sickness," Dr. Robert Glatter, an emergency physician at Lenox Hill Hospital in New York City, told Live Science in an email. People experiencing motion sickness often "seek colder temperatures or environments with improved air circulation, or choose options that cool our bodies down, when in fact the actual mechanism behind [nausea] involves a drop in our core body temperature," he said.

Related: What's the hottest temperature the human body can endure?

The hallmark symptoms of motion sickness are nausea, vomiting and sweating. Lesser known is that when a person gets motion sick, their core body temperature drops. They actually become slightly hypothermic. This phenomenon was first noticed about 150 years ago in sailors suffering from seasickness, but scientists began to study this phenomenon only in the last several decades, according to a study published in 2014 in the journal Temperature. 

Capillaries in the skin dilate during motion sickness, which allows more blood to flow through close to the skin's surface, losing heat to the environment and lowering core body temperature. This process goes hand-in-hand with breaking out into a sweat to further lower their body temperature, which a person may experience as a "cold sweat" since they're slightly hypothermic. 

When a motion-sick person's temperature drops, their central nervous system, specifically the hypothalamus, the part of the brain that regulates body temperature, tries to counteract the plunge. So although their core temperature is low, a nauseated, motion-sick person may actually feel hot and flushed.

This drop in temperature and the body's compensation reaction to it are actually what make a person feel nauseated, Glatter said. Getting cold air or placing a cool compress on the back of the neck or forehead for a few minutes can help reduce the feeling of being hot or flushed because it counteracts the hypothalamus' efforts to raise body temperature, thus easing the feeling of nausea.

Experts aren't quite sure why the temperature change associated with motion sickness occurs. One potential reason could be that at a lower temperature, tissues need less oxygen to survive, and it may be more difficult for a person to get enough oxygen when they're ill. However, it's "more likely an adaptive response influenced by poorly understood mechanisms at the cellular level," Glatter said.

Similarly, experts also aren't sure why the temperature drop and subsequent compensation to increase body temperature leads to nausea. One theory suggests that both the nausea and temperature change may be a natural way the body defends itself in response to toxins. Nausea often leads to vomiting, which can clear toxins from a person's system. So-called "defensive hypothermia" may also protect against toxins by conserving the person's energy so they can focus on fighting the invader, according to a 2016 review in the journal The Quarterly Review of Biology. 

"If we assume that the 'cold sweats' associated with nausea are a part of natural defense against poisoning or infection, lowering of body temperature after detection of a toxin could be part of an evolutionary approach that results in 'defensive hypothermia,'" Glatter said. According to the 2014 study, evidence that "defensive hypothermia" occurs during toxic shock in human and animal models supports this theory.

Originally published on Live Science.

COVID-19 may mess with the body's fight-or-flight response, a small new study suggests.

The coronavirus can infect many different organs in the body, including the brain. Previous studies have found that in rare cases, SARS-CoV-2 infections can lead to a variety of forms of brain damage including deadly inflammation, Live Science previously reported. In some cases, the virus has also been linked to "brain fog" and other psychiatric issues in patients, according to another Live Science report. 

But there's still much that’s unknown about the subtle impacts a typical COVID-19 infection may have on the nervous system. In the new study, researchers recruited a small group of young adults in the U.S. who were recovering or had recovered from COVID-19, to examine whether the coronavirus triggers changes in the sympathetic nervous system.

Related:  Coronavirus variants: Here's how the SARS-CoV-2 mutants stack up 

The sympathetic nervous system —  which regulates involuntary body functions such as blood pressure, pupil dilation and body temperature — drives the body's fight-or-flight response. In the face of danger, such as an approaching wild animal, the sympathetic nervous system will trigger the release of hormones to increase alertness and heart rate, which sends extra blood to the muscles, according to Live Science.

"'Fight-or-flight' is a great mechanism in situations of high stress," such as when a bear is chasing you, said study senior author Abigail Stickford, an assistant professor of health and exercise science at the Appalachian State University in North Carolina. "But when that system is chronically elevated or stimulated, it's not so great."

Stickford and her team recruited 16 previously healthy young adults who had tested positive for SARS-CoV-2 more than two weeks prior to visiting the lab and had mild cases. The researchers recorded nerve activity using electrodes, blood pressure and heart rate while the participants were resting and while the participants were sticking their hand into an ice water bath — a heart test known as a "cold pressor test." They compared their results to healthy young adult controls who weren't infected. 

The researchers found that young adults recovering from SARS-CoV-2 infections had elevated sympathetic activity while resting compared to healthy controls. But they had no difference in heart rate, blood pressure and sympathetic nerve activity during the cold pressor test. That means that their fight-or-flight response was more active when it didn't have to be during rest, but the system was still able to respond properly to a threat.

They also found that when the participants were asked to perform an "orthostatic challenge," or quickly stand from a sitting or lying down position, the participants recovering from SARS-CoV-2 infections had higher sympathetic nerve activity and a greater increase in heart rate compared to healthy controls.

Many experts speculate that COVID-19 impacts the sympathetic nervous system, based on heart rate data from those infected and reports of symptoms including racing heartbeat and cognitive changes, so the results weren't "entirely surprising," Stickford told Live Science in an email. "However, these participants were very young, healthy, and with mild symptoms, so in that regard, it was surprising."

The authors say that if the results hold true in older individuals who get COVID-19, "there may be substantial adverse implications for cardiovascular health."

Just SARS-CoV-2 or all viruses?

No one knows why or how the virus triggers changes in the sympathetic nervous system, but the virus triggers inflammation, which in turn is linked to elevated sympathetic nervous system activity, Stickford said. 

Still, that doesn't mean that other viruses aren't causing these changes as well.

Dr. Igor Vaz, from the University of Miami's Department of Medicine, who was not involved in the research, thinks that the results would have been more robust if the control group hadn't been healthy individuals but individuals recovering from a different viral infection, such as the flu. "Using the control group as healthy individuals misses the opportunity to show that" these complications are due exclusively to SARS-CoV-2, and not just because people are recovering from a viral infection, he wrote in a "letter to the editor," which was published in response to the study. 

In a response to the letter, the authors acknowledged that comparisons with other infections would have given more insight into the exact impact of SARS-CoV-2 on the nervous system, but that their "study design was the most appropriate starting place," given various limitations such as access to patient populations.

The biggest limitation of the study is that the researchers don't know what the participants' nervous system activity looked like prior to their COVID-19 diagnosis, Stickford said. But it's likely that the changes to the fight-or-flight response in this young, healthy population is temporary, Stickford added. As viral load decreases, inflammation in the body decreases, and "we would expect the [sympathetic nervous system] activity to also decline a bit," she said. 

The researchers are continuing to track these participants, none of whom developed "long COVID," a phenomenon whereby symptoms continue for months after a person is infected. 

Had these participants developed long COVID, "there would likely be more to the story," as people who suffer from long COVID continue to display symptoms that suggest a dysfunction of the nervous system.

The findings were published on June 26 in The Journal of Physiology.

Originally published on Live Science.

A mysterious neurological ailment first reported by U.S. personnel in Havana, Cuba, may be more widespread among diplomats, soldiers and spies than previously thought. 

More than 60 people have reported sudden episodes of nausea, dizziness and headaches from incidents overseas, The New York Times reported. In at least a few cases, the symptoms have been persistent, with ongoing problems such as vertigo and pain reported by personnel. 

The Biden administration is moving aggressively to investigate the reports, according to the Times. A 2020 report from the National Academy of Sciences (NAS) suggested that the ailment could be caused by a directed pulse of radio-frequency energy. (Radio-frequency energy includes radio waves and microwaves.)

Related: Spooky! Top 10 unexplained phenomena

"Studies published in the open literature more than a half-century ago and over the subsequent decades by Western and Soviet sources provide circumstantial support for this possible mechanism," NAS Committee Chairman Dr. David Relman wrote in the report. "Other mechanisms may play reinforcing or additive effects, producing some of the nonspecific, chronic signs and symptoms, such as persistent postural-perceptual dizziness, a functional vestibular disorder, and psychological conditions."

Reports of the neurological symptoms first began in 2016 with a series of cases among people working at the U.S. embassy in Havana. Since then, according to the Times, there have been reports in Russia, China, and other countries in Asia and Europe. In one case in Russia, a military officer reported pulling his car into an intersection and suddenly being hit with a wave of nausea and a painful headache. His 2-year-old, strapped in the backseat, started crying. When the officer pulled away from the intersection, the symptoms subsided and the child stopped crying, the Times reported. 

Some officials suspect Russia's military intelligence agency is behind the incidents, but the U.S. government is not ready to assign blame, according to the Times. 

"As of now, we have no definitive information about the cause of these incidents, and it is premature and irresponsible to speculate," Amanda J. Schoch, the spokeswoman for the Office of the Director of National Intelligence, told the newspaper. 

Officials are also investigating two incidents that occurred near the White House shortly after the presidential election of 2020, according to CNN. Two members of the National Security Council reported symptoms that struck suddenly near entrances to the grounds. The events happened several weeks apart and at different gates. 

Many of the episodes remain classified, making the task of uncovering potential causes of the ailment more difficult for scientists, the researchers wrote in the NAS report. Making matters more complicated, some sufferers reported sudden and transient symptoms, while others reported slow-developing, chronic problems. It was impossible to rule out different causes for different cases, Relman wrote.  

Within the Central Intelligence Agency (CIA), which has not disclosed the number of personnel affected, Deputy Director David Cohen has been assigned to meet with victims and brief Congress regularly, according to the Times. The agency has also assigned more medical personnel to manage the cases among CIA staff. An increasing sense of urgency is driving the governmental response, according to the Times: The latest report of a possible attack occurred within the past two weeks.

Originally published on Live Science.

The entire history of the animal kingdom is like a long highway, with different species exiting at different points to pursue their own evolutionary paths. And sea sponges got off at the highway's first exit, ending up in the most distant corner of the country.

Scientists recently compared the genetics of sponges with that of another unusual animal: comb jellies. They say their research, published March 19 in the journal Nature Communications, resolves a debate: Some biologists already considered sponges the most distant cousins of all other animals; others argued that comb jellies were the true "sister to all other animals."

The concept of evolution existed for about a century before anyone discovered DNA. Many of the ideas developed during that era still hold: Animals that share many traits likely diverged from common ancestors more recently — taking the same evolutionary route until that point. And two animals that share fewer traits likely diverged longer ago.

Humans and other great apes, for example, look and act alike. So it makes sense to assume they share relatively recent ancestors. People and dolphins look different and live very different lives, but they share some key traits — live birth, mammary glands and hair. So they're more like second or third cousins.

Taking this approach to the entire diversity of animals on Earth would suggest that sponges split off longest ago. They don't have muscles, nervous systems, organs or even the traditional mouth-to-anus digestive tract common to all other members of the animal kingdom. Their animal traits are basic: They're made of multiple cells, produce sperm, lack cell walls and need to eat for energy.

Related: 7 theories on the origin of life

Comb jellies, which have muscles, simple anuses and nerves despite so many other differences from most animal life on Earth, seem to have diverged more recently — belonging to the same non-sponge branch of animal life as human beings, sea lions and tarantulas.

This sort of analysis is useful but imperfect. Birds and bats both fly, but not due to any common ancestor; they evolved their wings independently, as Live Science previously reported. Manatees and whales are both water-dwelling mammals, but Live Science reported manatees are closer to elephants than ShamuIt seemed possible, based on earlier genetic work, that comb jellies split off from the rest of the animal kingdom before nervous system-less sponges did. As Live Science reported in 2017, most studies of relationships between animals look at their whole genomes. But this big-picture method is too imprecise to make fine distinctions between cousins as distant as sponges and comb jellies. So the most important sponge-comb studies rely on a handful of genes that all organisms share.

Even in these common genes, mutations creep in over time. The more mutations that separate two animals' common genes, the longer ago their evolutionary paths diverged. From this perspective, some scientists argued comb jellies and not sponges were the most distant cousins of other life. But that conclusion came from just a couple of genes that had diverged greatly in the comb jellies.

If comb jellies were the most distant cousins, that would be important. It would suggest comb jellies split off before nerveless sponges — and evolved their own nerves separately from other life. And if evolution invented the nervous system (or anus) twice, then maybe evolution really likes nervous systems (or anuses) for some reason. That would tell us something important about life itself.

This new paper throws cold water on that idea.

"Instead of comb jellies, our improved analyses point to sponges as our most distant animal relatives, restoring the traditional, simpler hypothesis of animal evolution," lead author and Trinity University microbiologist Anthony Redmond said in a statement.

The Trinity team developed a new method for studying the animals' genetics, taking into account the mechanisms of evolution itself. Genes contain instructions for building big, complex molecular machines known as proteins. When small pieces of a gene mutate — individual letters of genetic code swapping out for different units of code — those changes can result in proteins that don't do their job. So mutations that stick around tend to follow strict rules, changing the individual pieces of those proteins (known as amino acids) only in ways that don't usually cause the whole protein to stop working. 

There are 20 amino acids in genetic code. That list of 20 breaks up into smaller "bins" of four to six biochemically similar amino acids that might, for example, share the same positive or negative charge.. A mutation that swaps one amino acid for another in the same bin is less likely to significantly change the behavior of a protein. Most mutations that stick around long enough to become part of a type of animal's genome involve swaps within bins.

Swapping an amino acid for a counterpart from a different bin is more likely to change the function of a protein. That means it's more likely to be harmful and therefore more likely to get weeded out through natural selection. Swaps of amino acids from different bins do happen, but it's much rarer that they stick around through the generations. 

So, to simplify matters, if every additional swap of amino acids from the same bin means two species diverged a generation further in the past — great grandparents rather than grandparents — a mutation that swaps an amino acid for another from a different bin might suggest a hundred generations. Accounting for the differences between types of mutations when studying sponge and comb jelly genomes suggests sponges, not jelly combs, diverged first from the rest of animal life.

While jelly combs do have those couple of genes that are radically divergent from other animals, suggesting they diverged long ago in the deep past, a more holistic look at the types of mutations present in their genomes suggests a more recent diversion than the one sponges took. Nerves, anuses, and other common features of non-sponge animal life likely only evolved once.

Originally published on Live Science.

Carnivorous plants known as Venus flytraps (Dionaea muscipula) lure insects between their blushing leaves with a fragrant nectar. When these insect-hungry plants snap down on their unassuming prey, they generate a measurable magnetic field, according to a new study.

The plant's magnetic field is more than a million times weaker than Earth's. Rather than serving a function for the plant this magnetic field is likely a byproduct of electrical energy that flows through its leaves, said lead author Anne Fabricant, a doctoral candidate at Johannes Gutenberg University Mainz and the Helmholtz Institute Mainz in Germany. Still, it's one of the first such fields ever detected in plants. 

"Wherever there is electrical activity, there should also be magnetic activity," Fabricant told Live Science. The laws of electromagnetism dictate that anything with an electrical current also generates a magnetic field; and that includes humans, animals and plants. In fact, it's such a common phenomenon among living things that there's a name associated with it: biomagnetism. But while much research focused on such magnetic fields in humans and animals, not much has been done to understand biomagnetism in the plant world.

Related: Image gallery: carnivorous plants

In the new study, Fabricant and her team used tiny glass sensors called "atomic magnetometers" that contain a vapor of atoms that are sensitive to magnetic fields, according to a statement. They then triggered electrical energy, in the form of an action potential, to flow through the Venus flytrap. Action potentials, which also occur in animal and human nervous systems, are bursts of electrical energy that allow cells to communicate.

Action potentials serve a "vital" function for the Venus flytrap, triggering the plant to close its leaves around insects that touch sensitive hairs on the plants' leaves, Fabricant said.

But the researchers stimulated the plant in another way, by using heat. They found that when stimulated, the Venus flytrap created a magnetic field up to a strength of 0.5 picotesla. That's  similar to the levels generated by nerve impulses in animals, according to the statement.

Magnetic fields have only been detected in two other plants prior to this study, a single-cell algae and a bean plant, Fabricant said. But those were measured using superconducting-quantum-interference-device (SQUID) magnetometers, which are just as bulky as their name and need to be cooled to extremely low temperatures, she said.

"It's exciting to demonstrate plant-biomagnetic measurements using atomic magnetometers, which operate at room temperature and can be portable and miniaturized," Fabricant said. "The fact that we were able to detect magnetic fields gives some hints about how electric currents are distributed in the trap." The researchers hope to measure even tinier magnetic fields in other plant species, according to the statement. 

The findings were published Jan. 14 in the journal Scientific Reports.

Originally published on Live Science.

No, you're not looking at a psychedelic Millennium Falcon: This flickering, ghostly image is the most detailed view of a mouse brain ever seen.

Researchers at the Allen Institute for Brain Science, a Seattle nonprofit dedicated to neuroscience, have been painstakingly recording every brain cell and every connection between those neurons in mice for the past several years. The result represents major progress since an earlier, simpler map they released in 2016. The now-complete map encompasses about 100 million cells, the institute reported in a paper published today (May 7) in the journal Cell.

The project aims to do for neuroscience what whole-genome sequencing did for biology in the 1990s: create a common, standardized mouse brain that all researchers working on mice can reference.

Related: 2016 Images reveal a first effort to map the mouse brain

"In the old days, people would define different regions of the brain by eye. As we get more and more data, that manual curation doesn't scale anymore," Lydia Ng, an Allen Institute researcher and senior author of the Cell paper, said in the statement.

Typically, researchers trace connections between brain cells using thin slices of tissue that can be imaged and explored layer by layer. To build a comprehensive, three-dimensional map, the Allen Institute team instead broke the mouse brain into "voxels" — 3D pixels — and then mapped the cells and connections within each voxel.

The result comprises an "average" of the brains of 1,675 laboratory mice, to make sure the map was as standard as possible. 

Mice are common "model organisms" in neuroscience. Their brains have fairly similar structures to humans', they can be trained, they breed easily, and researchers have already developed robust understandings of how their brains work. 

The hope is that the map will bring that understanding to a new level, the Allen Institute said. In doing so, neuroscientists will have a tool with which to develop new research programs and accelerate research already underway. The institute compared its achievement to 1990s-era efforts to sequence different organisms' DNA for the first time, projects that transformed the way biologists work

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Originally published on Live Science.

In 2008, archaeologists were stunned to discover a human brain dating to the Iron Age. The finding seemed to defy basic biology; human brains, like any other soft tissue, typically decay soon after death. 

But now, scientists have figured out how this brain remained intact for 2,600 years. 

Multiple factors, they said in their new study, played a role, including the person's tightly folded brain proteins and the way in which the person was buried in what is now York, England. 

Related: Photos: Stone Age Skulls Found on Wooden Stakes

The so-called "Heslington brain" made headlines after the York Archaeological Trust excavated its mud-covered skull in the village of Heslington and found the well-preserved brain inside. "Although covered by sediment, individual brain gyri became discernible after cleaning," the researchers wrote in the study. Radiocarbon dating indicated the individual had lived around 673 B.C. to 482 B.C.

Whoever buried the mysterious person didn't use any artificial preservation techniques, the scientists noted. Rather, it appears that the way in which the person was buried made a key difference. It's also possible that an unknown disease altered the person's brain proteins before he or she expired, the researchers said.

"The manner of this individual's death, or subsequent burial, may have enabled the brain's long-term preservation," study lead researcher Axel Petzold, an associate professor at the University College London Queen Square Institute of Neurology, said in a statement.

Petzold has spent years studying two types of filaments in the brain: neurofilaments and glial fibrillary acidic protein (GFAP), both of which act like scaffolds that hold brain matter together. When Petzold and his team looked at the Heslington brain, they saw that these filaments were still present, raising the idea they played a role in the brain's extraordinary preservation, he said. 

In most circumstances, brains rot after enzymes from the environment and the dead person's microbiome eat up the tissue. But for the Heslington brain, it's possible that these enzymes were deactivated within three months, according to experiments the researchers did. In these tests, Petzold and his colleagues found that it takes about three months for proteins to fold themselves into tight aggregates if these enzymes are not present.

Perhaps an acidic fluid invaded the brain and prevented these enzymes from causing decay before or just after the person died, Petzold said. He added that this enigmatic person likely died after being struck in the head or neck, hanged or decapitated.

Typically, neurofilament proteins are found in greater concentrations in the white matter, located in the inner parts of the brain. But the Heslington brain was an anomaly, with more filaments in the outer, gray matter areas. It's possible that whatever stopped the enzymes from decomposing the brain began on the outer regions of the brain, like an acidic solution seeping into the brain, Petzold said.

The finding may provide insight into treatment for Alzheimer's disease. The team looked at how long it takes brain protein aggregates to unfold themselves, finding that it took an entire year. This suggests that treatments for neurodegenerative diseases that involve protein aggregates may need a more long-term approach than previously thought.

This isn't the only ancient human brain tissue archaeologists have found. For instance, roughly 8,000-year-old brain material was found inside human skulls that had received an underwater burial in Sweden. That said, the Heslington brain is among the best preserved ancient human brains, the researchers said.

The study was published Jan. 8 in the Journal of the Royal Society Interface.

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Originally published on Live Science.

Inky stains found in fossils of 500-million-year-old bug-like creatures may be beautifully preserved, symmetrical brain tissue. The fossil find may help lay a heated scientific controversy to rest — the question of whether brains can be fossilized.

Scientists discovered these splotchy marks in fossils of  the arthropod Alalcomenaeus, an animal which shares its phylum with modern insects, spiders and crustaceans. The animals lived during the Cambrian period, which took place between about 543 million and 490 million years ago, and sported a tough exoskeleton that fossilized well. But the soft tissues of the creature's brain and nerves often decayed and therefore disappeared from the fossil record. 

Now, a new study, published Dec. 11 in the journal Proceedings of the Royal Society B, describes not one but two Alalcomenaeus fossils complete with brains and all their trimmings.   

"What we are dealing with in the fossil record are exceptional circumstances. This is not common — this is super, super rare," said co-author Javier Ortega-Hernández, an invertebrate paleobiologist at Harvard University and curator of the Harvard Museum of Comparative Zoology. Previously, paleontologists have identified only one other Alalcomenaeus specimen thought to have nervous tissue, but the finding was met with skepticism. With two more specimens in hand, scientists can now be confident that nervous tissue can in fact be fossilized and found in exceptional Cambrian arthropod fossils, Ortega-Hernández said.

Related: In Photos: These Bizarre Sea Monsters Once Ruled the Ocean

Long-standing debate 

Besides Ortega-Hernández and his team, only a handful of researchers have reported finding fossilized nervous tissue in Cambrian-period arthropods. In a 2012 paper, scientists described the first evidence of a fossilized arthropod brain, in a tiny creature called Fuxianhuia protensa. Although widely covered in the media, the report attracted critics.       

"They said, 'Rubbish, lot of nonsense,'" said Nicholas Strausfeld, a regents professor in the department of neuroscience at the University of Arizona and co-author of the 2012 study, as well as several others on brain-like features in arthropods. Some paleontologists argued that, based on our understanding of how animals decay, the stained specimens Strausfeld and others unearthed couldn't possibly contain nervous tissue, Strausfeld said. Some theorized that the brain stains must be either a strange fluke of fossilization or fossilized beds of bacteria, known as biofilms.  

But now, the new study by Ortega-Hernández and his colleagues serves as "a really pleasing validation of earlier work," Strausfeld told Live Science. "He's put to rest a lot of objections from people."

In their study, Ortega-Hernández and his co-authors uncovered a new Alalcomenaeus fossil buried in Utah within a region of geological depressions known as the American Great Basin. The authors noted symmetrical stains along the creature's midline that resembled nervous system structures found in some modern arthropods, including horseshoe crabs, spiders and scorpions. "The nervous system and the gut kind of cross each other, which is really funky but common in arthropods nowadays," Ortega-Hernández told Live Science.  

Related: Weird and Wonderful: 9 Bizarre Spiders

The stains also contained detectable levels of carbon, a key element in nervous tissue. The dark splotches also plugged into the animal's four eyes, as would be expected for nervous system tissue. Having checked all these criteria, Ortega-Hernández said that he could confidently report finding fossilized nervous tissue in the newfound specimen. 

But to double-check their findings, the authors also examined a second Alalcomenaeus fossil from the American Great Basin. Originally dug up in the 1990s, the specimen sported similar stains and carbon traces to the newfound fossil. What's more, both Great Basin fossils matched descriptions of another specimen that Strausfeld found in China. All three fossils had been found buried in similar deposits, indicating that a unique preservation process allowed all their brain matter to fossilize, Ortega-Hernández said.      

Counterarguments

Although Ortega-Hernández and his colleagues checked and double-checked their work, the authors "generally have to be cautious about claiming to have found a genuine fossil brain," Jianni Liu, a professor at the Early Life Institute in the Department of Geology at Northwest University in Xi'an, China, told Live Science in an email. Liu argues that the blobby stains seen in Cambrian fossils might be a "slightly random effect of the decay process" rather than remnants of brain matter. 

In a 2018 study, Liu and her colleagues examined about 800 fossilized specimens and found that nearly 10% contained inky stains in the head region. The authors reviewed previous studies of animal decay and found that nervous tissue tends to decay quickly, but gut bacteria can stick around and "produce these so-called biofilms as radiating [stains] which look a bit like parts of a nervous system," Liu wrote. 

Related: 5 Ways Gut Bacteria Affect Your Health

Several paleontologists, including Strausfeld, pointed out that Liu failed to examine fossils that reportedly contained brain tissue, and that lack of primary evidence marks a "major shortcoming" in her study. What's more, the specimens Liu did examine contained asymmetric stains rather than symmetric ones, meaning they would not have been interpreted as brain tissue anyway, Strausfeld said. 

Additionally, studies of decay often measure tissue breakdown in water, whereas buried fossils interact with a multitude of chemicals carried in the sediment around them, Ortega-Hernández said. For instance, some studies suggest that a combination of clay and water jump-starts a "chemical tanning" process that toughens soft tissues in the body, similar to how particular chemicals can transform supple cow hide into leather, Ortega-Hernández said. 

More work must be done to clarify the role of sediment in fossil preservation, but as of now, ample evidence suggests that arthropod remains placed under intense pressure solidify over time, Strausfeld said. The brain and nerves within the animal flatten out in the process, and because nervous tissue contains lots of fat, the structures repel water and "have some resistance against decay," he said.

Despite the evidence in their favor, Ortega-Hernández, Strausfeld and their colleagues may need to dig up a lot more arthropod brain bits to convince naysayers that ancient brains can fossilize.         

"We appreciate the authors' efforts to justify their results as being genuine nervous tissue, but remain sceptical while the data comes from only two fossils," Liu said. "New data is always welcome, but as we noted previously, we would be more convinced if the anatomical features appeared in a consistent form across several specimens independently."

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Originally published on Live Science. 

Scientists have found a previously unknown organ lurking under the skin, and it may help you feel the pain of a pinprick.

It was previously thought that people perceive the pain of a pinprick via nerve endings that sit right below the outer layer of the skin. Now, a new study suggests that it's not just nerves, but nerves tangled up in special cells that make us flinch.

"We have known for a long time that there are various kinds of sensory organs in the skin, but those that we've been aware of have only been involved in touch sensation," said study senior author Patrik Ernfors, a professor of tissue biology at the Karolinska Institute in Sweden. 

This mesh of branched cells and nerves is a newfound "sensory organ" because it responds to external cues and relays that information to the brain. Unlike other known sensory organs under the skin, this one plays a role in pain perception, Ernfors told Live Science.

Related: Top 3 Techniques for Creating Organs in the Lab 

This sensory organ is sensitive to pricks or jabs, and once activated by pressure, the organ sends signals to the brain. The brain then sends signals down to the site of the prick that tells us to feel pain.  

The cells that make up this organ, called Schwann cells, each look "a little bit like an octopus," with long, tentacle-like protrusions extending into surrounding nerves, Ernfors said. Schwann cells are generally known to surround and insulate nerves.

But to figure out the function of these specific Schwann cells in the skin, researchers tested what happened when they were turned off in mice; to do so, the scientists used a method called "optogenetics." They inserted a light-absorbing protein into the genomes, and this protein turned the Schwann cells "on" when enough light was absorbed. 

When the cells were activated, the mice withdrew their paws, which indicated that they felt pain. The mice also displayed coping behaviors, such as licking and shaking their paws. Just like "if you burn yourself, you flush your hand under cold water,"  the mice were trying to soothe the pain, Ernfors said.

"When we turn these cells off, the animals feel much less pressure and pain" in response to painful pricking sensations than do typical mice, Ernfors said. However, when researchers turned off these cells and then tested the animals for cold and heat sensitivity, the mice could sense those sensations equally well as when the cells were not turned off. 

That means the nerves themselves are "probably much more important than the terminal Schwann cells are for heat and cold sensation," while the Schwann cells are more important for pressure sensations, Ernfors said. 

Under the microscope, these Schwann cells rapidly activate and send signals to other nerves when they are poked. Now, Ernfors wants to find if these cells have anything to do with chronic pain, he said. 

"Chronic pain has become a focus of attention as opioid addiction continues to debilitate lives and cause mortality," wrote graduate student Ryan Doan and senior scientist Kelly Monk, from the Vollum Institute in Oregon, in a commentary accompanying the study.

The octopus-like Schwann cells are "a new potential target cell for pain medication," Doan and Monk wrote.

The findings were published on Aug. 16 in the journal Science.

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Originally published on Live Science.

When an octopus coils one of its flexible arms around a rock or a bit of food, it's not because the animal's brain said, "Pick that up." Rather, the arm decides for itself what it's going to do next. For a person, that would be like having one's big toe call the shots about where they're going to walk.

But a cephalopod's nervous system isn't wired like a human's — or like the systems found in any other vertebrates, for that matter, where a central brain broadcasts marching orders to the rest of the body. Instead, octopus limbs are studded with concentrations of neurons called ganglia; these "arm brains" can therefore operate independently of the central brain.

In fact, scientists who recently visualized progressive movement in octopus arms discovered that the animal's central brain is hardly involved at all; they presented their findings June 26 at the 2019 Astrobiology Science Conference. [8 Crazy Facts About Octopuses]

The researchers used a camera and behavioral-tracking software to model how an octopus perceives and then processes information about its environment using its arms, Dominic Sivitilli, a graduate student in behavioral neuroscience and astrobiology at the University of Washington in Seattle, explained during the presentation.

"What we're looking at, more than what's been looked at in the past, is how sensory information is being integrated in this network while the animal is making complicated decisions," Sivitilli said in a statement.

An octopus's arm movement begins far away from the brain, triggered by sensors in a groping arm sucker feeling around on the seafloor or in an aquarium. Each sucker contains tens of thousands of chemical and mechanical receptors; to put that into perspective, a human fingertip holds just a few hundred mechanical receptors, Sivitilli said.

When an octopus touches something interesting, the "brain" in its arms processes the input and moves the signal along, telling the arm what to do next. Signals generated by one sucker are passed to its closest neighbor, activating arm muscles and generating a sweeping wave of motion that travels up the arm toward the body, the researchers discovered. While the arms are actively engaging with the environment — and with each other — the signal that reaches the animal's central brain is "highly abstracted" and not directly involved with arm interactions, Sivitilli explained.

Essentially, octopuses "outsource" computation about how to move their bodies, assigning those actions to local controls — ganglia — in each arm, rather than relying on the central brain to tell the arms what to do, Sivitilli said in the presentation.

"In a way, the octopus has sent its mind out into the environment to meet it halfway," he added.

But wait, you might be thinking — why are scientists talking about octopuses at an astrobiology conference? What does this have to do with extraterrestrial life? (And no, it's not because octopuses are really space aliens, as another group of researchers claimed in 2018.)

Octopuses are thought to be highly intelligent, yet their workarounds for perceiving and interacting with the world around them differ dramatically from techniques that evolved in intelligent vertebrates. Octopus cognition could therefore serve as an important alternative model for understanding intelligence, and it could prepare experts for recognizing unusual expressions of intelligent life that originated on other worlds, Sivitilli said in the statement.

"It gives us an understanding as to the diversity of cognition in the world," Sivitilli said. "And perhaps the universe."

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Originally published on Live Science.

One person has died in connection with a Listeria outbreak tied to sliced deli meats and cheeses, according to health officials.

The outbreak, which was announced on Wednesday (April 17), has sickened a total of eight people in four states (Michigan, New Jersey, New York and Pennsylvania), according to the Centers for Disease Control and Prevention (CDC). All eight patients needed to be hospitalized. The death occurred in a patient in Michigan.

Listeriosis, caused by the bacterium Listeria monocytogenes, is the most deadly foodborne illness. Although serious illness with Listeria is rare, for people who do get sick, the infection can be particularly lethal: An estimated 1,600 illnesses and 260 deaths from the bacterium occur each year in the U.S., according to the CDC.

But why is Listeria so dangerous?

It's important to note that Listeria typically isn't dangerous for most people. Rather, the bacteria typically only cause symptoms in people with weakened immune systems — such as pregnant women and older adults — who already have a reduced ability to fight any kind of infection, said Dr. Amesh Adalja, a senior scholar at The Johns Hopkins Center for Health Security in Baltimore.

But unlike many other types of foodborne illnesses, Listeria also has the ability to get into people's central nervous system, leading to particularly serious complications.

"The fact that it has this ability to get into the central nervous system makes it more deadly," Adalja told Live Science. "When you get an infection in the central nervous system, it's much more serious than one that's restricted to the GI [gastrointestinal] tract." [Top 7 Germs in Food that Make You Sick]

Once inside the central nervous system, Listeria can cause infections in the membranes surrounding the brain and spinal cord (known as meningitis), or the brain itself (known as encephalitis). Both of these complications can be life-threatening.

Pregnant women are 10 times more likely to become infected with Listeria than the general population, according to the American College of Obstetricians and Gynecologists (ACOG). In these cases, the infection poses a risk not only to the woman, but also to the fetus, potentially causing miscarriage, stillbirth or preterm labor, ACOG says. For these reasons, pregnant women are told to avoid deli meats and other foods that are more likely to contain Listeria bacteria, such as unpasteurized milk and foods made with unpasteurized milk, including soft cheeses.

In the current outbreak, patients reported eating sliced deli meats and cheeses before becoming ill. Infections have occurred as far back as November 2016 and as recently as February and March of this year.

Officials have identified the outbreak strain of Listeria (the strain making people sick) in samples of deli meat in various stores. However, officials have not identified a common supplier of deli products tied to the outbreak.

At this time, the CDC is not telling people to avoid eating deli products. But the outbreak is a reminder that people at high risk for Listeria infection — including pregnant women, adults ages 65 and over and those with weakened immune systems — should be cautious about eating and handling deli meats and soft cheeses. The CDC recommends that people in this group avoid eating hot dogs, lunch meats, cold cuts and other deli meats, unless they are heated to an internal temperature of 165 degrees Fahrenheit (74 degrees Celsius) or until steaming hot. People in this group should also avoid eating soft cheeses unless they are labeled as being made with pasteurized milk.

Symptoms of Listeria infection can include fever, muscle aches, nausea, diarrhea, headache, stiff neck, confusion, loss of balance and convulsions, according to the CDC.

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Originally published on Live Science.

In an apparent world first, veterinarians have successfully performed a spinal tap on a live dolphin.

That dolphin, who underwent the procedure at SeaWorld San Antonio, is named Rimmy. She is a bottlenose dolphin, about 3 or 4 years old, who was rescued from Texas' Sea Rim State Park off the Gulf of Mexico, where she was found sick and stranded in 2017.

While trying to diagnose the cause of Rimmy's stranding, vets saw that the dolphin was riddled with ailments, including pneumonia and "nasal parasites," Dr. Hendrik Nollens, vice president of SeaWorld's veterinary services, told ABC News. [Deep Divers: A Gallery of Dolphins]

Rimmy spent the next 14 months being treated at a special rehab center for stranded marine mammals, where researchers from the National Oceanic and Atmospheric Administration (NOAA) decided she was too fragile and dependent on humans to return to the wild.

Before Rimmy could find a new home in captivity among other dolphins, however, she had to be tested for an infectious animal bacteria called Brucella, which can result in a several symptoms, including reproductive loss. When one of several tests came back positive, Rimmy's caretakers decided they needed to be 100 percent certain before deciding the dolphin's fate. If she had Brucella, she might not be able to ever interact with other dolphins, Nollens said.

The vets decided that Rimmy needed a lumbar puncture, commonly known as a spinal tap. — The procedure is used to collect cerebrospinal fluid, in order to diagnose diseases of the central nervous system. To keep Rimmy perfectly still for her spinal tap, vets anesthetized her. When Rimmy was unconscious, vets inserted a long, thin needle into the dolphin and collected a sample of spinal fluid for testing.

Good news: The results showed that Rimmy was "free and clear" of any bacteria, and that nothing was stopping her from living out the next chapter of her life among fellow dolphins.

• In Photos: A Rare Albino Risso's Dolphin
• In Photos: The World's Most Endangered Marine Mammal
• The 10 Weirdest Sea Monsters

Originally published on Live Science.

Almost everyone will be familiar with the comical sight of a baby who suddenly elicits a violent shudder: It's a pretty reliable indicator that the infant needs a diaper change. That's because peeing is oddly associated with shivering — a strange phenomenon that persists even into adulthood. But what's going on inside our bodies to generate this unusual response to a basic, daily function?

The truth is that we don't really know. There's no peer-reviewed research on the subject to shed light on the precise biological underpinnings of this phenomenon. But from what scientists do know about the bladder and its relationship with the nervous system, they've pieced together some possible explanations for why we shiver when we pee.

These center on two main ideas: It's caused either by the sensation of the drop in temperature as the warm pee leaves your body or by a confusion between signals in the autonomic nervous system (ANS). [Why Does Asparagus Make Your Pee Smell Funny?] 

The first idea is founded on the common-sense fact that we typically shiver when we feel a sudden chill. As far as peeing is concerned, the logic goes that when we expose our nether regions (an obvious necessity for peeing) to cool air, and then simultaneously void the body of warm liquid, it creates an internal temperature imbalance — a chill — that triggers an uncontrollable shiver.

But some scientists aren't convinced by this idea, including Dr. Simon Fulford, a consultant urologist at the James Cook University Hospital in the United Kingdom. He prefers the alternative theory, which digs deeper into the nervous system for clues.

The process of urination is overseen by the ANS, the control center that orchestrates many automatic bodily functions, such as temperature and the beating of a heart, Fulford said. Obviously, urination isn't entirely automatic because we do have voluntary control over when we pee. But before that crucial decision point, urination is largely governed by two parts of the ANS, called the parasympathetic nervous system (PNS), and the sympathetic nervous system (SNS).

When the bladder reaches fullness, tiny stretch receptors in its muscular wall detect the motion of the bladder stretching and activate a set of nerves in the spinal cord called the sacral nerves. In turn, these spring the PNS into action, which causes the muscular bladder wall to contract, preparing it to push urine out of the body. This autonomic process works like an on-off switch, suppressing the instructive nerve reflexes while the bladder is still filling up, but "stimulating those reflexes to act when the bladder is full," Fulford told Live Science.

An odd quirk of this arrangement is that when urine leaves the body, blood pressure drops. "There does seem to be good evidence that blood pressure rises slightly with a full bladder, and that this drops on voiding, or soon after," Fulford said.

What happens next is difficult to untangle, biologically speaking. But it seems that this sudden dip in blood pressure spurs a reaction from the sympathetic nervous system, a part of the ANS that is involved in the body's fight-or-flight response. The SNS regulates many factors, including blood pressure, as part of this reaction. Experts already know that when the SNS detects low blood pressure, it releases a series of neurotransmitters called catecholamines, which among their many functions, will carefully restore blood pressure to its former balance across the body. When it comes to urination, it's possible that this sudden surge of catecholamines causes the pee twitch. [Why Do People 'Twitch' When Falling Asleep?]

But why? For reasons that aren't fully understood, the interaction between the two nervous system components — the release of urine, fine-tuned by the PNS, and the surge in catecholamines, orchestrated by the SNS — may be causing mixed signals in the nervous system. That seems to trigger a glitch in the system that makes us shudder involuntarily.

Fulford says a similar phenomenon called autonomic dysreflexia sometimes occurs in patients with a spinal cord injury. This happens when a stimulus, like a full bladder, occurs below the site of the spinal injury, resulting "in an excessive autonomic nervous system response that causes the blood pressure to climb rapidly, the pulse rate to drop and patients to flush and sweat," he explained. This incongruous reaction echoes the weird shivers that we get when we pee.

Another clue is that men seem to experience this phenomenon more than women do, which might be explained by the fact that men usually stand when they urinate — possibly intensifying the dip in blood pressure that's thought to precede the shudder.

Whatever the cause, this bodily oddity shouldn't be a cause for concern. "There's not been any substantial research on this subject, but it's a normal bodily function and nothing to worry about," Dr. Grant Stewart, an academic urological surgeon at Cambridge University in England and chair of The Urology Foundation's Science and Education Committee in the United Kingdom, told Live Science.

• In fact, all men really have to worry about is getting their aim right when the shivers strike.

Original story on Live Science.

You're reading these words because you have a brain in your head. But did you know you also have a brain in your butt?

OK, not a literal brain — more of an autonomous matrix of millions of neurons that can, somehow, control intestinal muscle movements without any help from your central nervous system. And these neurons don't actually live in your butt, but they do live in your colon, or large intestine — that tube-like organ that connects the small intestine to the rectum and shepherds what remains of the food you ate through the final leg of the digestive tract.

Scientists call this site of colon intelligence your enteric nervous system, and because it can function without instructions from the brain or spine, some scientists like to call it your "second brain." How smart is this autonomous, intestinal brain? Scientists don't know for sure yet. But according to a new study in mice, published May 29 in the journal JNeurosci, the answer might be pretty smart for an intestine.

"The enteric nervous system (ENS) contains millions of neurons essential for organization of behavior of the intestine," wrote the team of researchers from Australia who observed the so-called second brain hard at work using a combination of high-precision neuronal imaging techniques.

When the researchers stimulated isolated mouse colons with mild electric shocks, they saw "a novel pattern of rhythmic coordinated neuronal firing" that corresponded directly to muscle movements in nearby sections of the large intestine.

These rhythmic, synchronized blasts of neuron activity likely help to stimulate specific sections of intestinal muscles at a standard rate, the researchers wrote. This ensures that colonic muscle contractions — also known as "colonic migrating motor complexes" — keep fecal matter moving in the right direction (out of the body, that is), and at a steady pace.

"This revealed that activity in the ENS can temporally coordinate [muscle] activity over significant distances along the length of [the] colon," the team wrote.

According to the researchers, similar synchronized neuron routines are also common in the early stages of brain development. This could mean that the pattern they identified in the colon is a "primordial property" held over from the early stages of the enteric nervous system's evolution.

But it could be even more important than that: Because some scientists hypothesize the enteric nervous system actually evolved before the central nervous system, the neuron firing pattern in your colon might represent the earliest functioning brain in your body. Yes, that would mean the brain in your butt could actually be your "first brain," not your "second brain." If this is true, you could say mammalian brains evolved first to move poop, and then to take care of more complex business.

However, this is the first time such a neuron-firing pattern has ever been detected in the colon, and so far, it's been found only in mice. The researchers are confident that their findings could apply to other mammals, too. But a clearer understanding of the enteric nervous system's power in humans will require further study — and lots of serious thinking from both brains.

Originally published on Live Science.

Just flicking on a light might one day provide pain relief to some patients with chronic pain, early research in animals suggests.

The research focused on a type of chronic pain called neuropathic pain, which results from damage to or dysfunction of the nervous system, according to the Cleveland Clinic. People with this condition may experience severe pain from even the lightest touch — for example, if something gently brushes against their skin.

In the new study, researchers in Italy first identified the type of nerve cell that appears to cause this sensitivity to gentle touch in mice. Then, they developed a light-sensitive chemical that binds to this nerve cell.

When mice with neuropathic pain were injected with this chemical, and then had a near-infrared light shined on their bodies, the treatment appeared to lead to pain relief. Normally, mice with neuropathic pain would quickly withdraw their paws when they were gently touched, but after the therapy, the mice showed normal reflexes upon gentle touch, the researchers said. [5 Surprising Facts About Pain]

The light therapy works by clipping off the nerve endings of the targeted cells, thus desensitizing them. "It's like eating a strong curry, which burns the nerve endings in your mouth and desensitizes them for some time," study leader Paul Heppenstall, a group leader at the European Molecular Biology Laboratory in Rome, said in a statement.

The therapy specifically targets the nerve cells that are sensitive to gentle touch. Other nerve cells — such as those that sense vibrations, cold or heat — are not affected by the light therapy, the researchers said.

The treatment is temporary; in the mice, the nerve endings grew back after about three weeks, and the animals became sensitive to gentle touch again.

Because the new study was done in mice, much more research is needed to see if the therapy will also provide pain relief to people with neuropathic pain. For instance, the researchers still need to confirm that the cells that cause sensitivity to gentle touch are the same in mice and people, and examine the safety of the treatment.

"A lot of work needs to be done before we can do a similar study in people with neuropathic pain," Heppenstall said. But the researchers want to develop the technology further," with the hope of one day using it in the clinic," he added.

The study was published today (April 24) in the journal Nature Communications.

Original article on Live Science.

Your brain keeps making new nerve cells, even as you get older.

That's a big deal. For decades, researchers believed that aging brains stop making new cells. But recent research has offered strong evidence to the contrary, and a new paper published today (April 5) in the journal Cell Stem Cell tries to put the notion to bed entirely. Aging brains, the researchers showed, produce just as many new cells as younger brains do.

"When I went to medical school, they used to teach us that the brain stops making new cells," said lead study author Dr. Maura Boldrini, a neurobiologist at Columbia University. [10 Surprising Facts About the Brain]

But, Boldrini told Live Science, researchers began to suspect that was wrong: Studies in mice showed that even the older mice produced new nerve cells. And early studies in humans started to turn up similar results.

This study, though, is the first to thoroughly track the brain's cell production over the course of a typical human lifetime.

Boldrini and her colleagues studied 28 brains that came from the corpses of healthy people ages 14 to 79. And these donated brains were unusual in this kind of research: The researchers knew a whole lot about them.

("Healthy" is, of course, a relative term. The brains were dead. But they didn't show evidence of any major disorders. And they didn't come from drug users. They also didn't come from people who had been treated with antidepressants, which researchers believe can actually stimulate cell growth.)

They came from a library of donor brains assembled at Columbia that had all been preserved using the same methods and that had detailed medical histories attached to them.

Boldrini and her colleagues sliced the hippocampi, an area of the brain important for learning and memory, into slivers, and counted the number of newly formed cells — those that had yet to fully mature — under a microscope.

This part turned out to be especially challenging. "People who study mice with tiny brains, it's easy," Boldrini said. "You cut them up, look at the cells, and you count them."

But human brains are bigger and more complicated. Boldrini and her colleagues used specialized computer software to count the cells under a microscope.

The older brains weren't completely unchanged. While they had as many new cells as younger brains, they seemed to be making fewer new blood vessels, and not forming new connections between brain cells as quickly.

It's important to note that the science of brain-cell formation in old age is far from mature. As recently as March 7, a paper published in the journal Nature challenged this idea that older brains keep making new nerves. In studies of sick and healthy brains, the authors found a sharp decline in the production of new brain cells, beginning around adolescence, with no new nerve cells detected in the brains of adults.

Boldrini suggested that the difference between her team's results and those of the Nature paper could have been traced to the brains the different groups were examining, and the methods used to examine them. The brains described in the Nature paper, she said, came from a wider range of people with different health conditions, including epilepsy, and may have been preserved using different techniques. Those preservation techniques, she said, may have destroyed evidence of new cells.

Because all the "healthy" brains in the Columbia study exhibited new cell growth, Boldrini and her team suggested that the continued ability to produce new cells in the hippocampus might be a key feature of brains that remain healthy into old age.

Originally published on Live Science.

A nerve agent was likely used to poison a Russian ex-spy and his daughter in England, new reports suggest.

The former spy, Sergei Skripal, 66, and his daughter, Yulia, 33, were found slumped on a park bench in Salisbury, England, on Sunday (March 4). Both Skripals allegedly looked pale and stiff; vomit was pouring from Sergei's mouth while his daughter sat frothing at the mouth with wide-open eyes, according to U.S. News and World Report.

According to investigators, the condition in which the Skripals were found indicates they were poisoned by a nerve agent — the most toxic and fast-acting chemical warfare agents in the world, Live Science previously reported. But what are nerve agents, and what do they do to humans? 

Related: 5 lethal chemical warfare agents

Simply put, nerve agents stop the central nervous system from communicating with the muscles, organs and glands it needs to keep your body's internal machinery running smoothly.  Specifically, the chemicals in nerve agents stop the body from breaking down a neurotransmitter called acetylcholine. The nervous system releases this crucial enzyme to activate muscles; when acetylcholine can't be broken down, those muscles — including the heart and lungs — spasm uncontrollably until they exhaust themselves, becoming effectively paralyzed.

Victims of nerve agents thus lose control of their bodily functions. Unintentional drooling, vomiting and urinating are common symptoms of exposure. Within minutes, the effects can escalate to asphyxiation or cardiac arrest. According to the Centers for Disease Control and Prevention (CDC), the extent of the poisoning increases with the amount and the duration of nerve agent exposure. Nerve agents typically enter the body through the mouth or nose, but can also be absorbed through the skin.

"If you have ever seen a fly sprayed, it drops on its back and lies with its legs in the air, twitching, this is the result of nerve agents taking hold," Dr. Simon Cotton, a senior chemistry lecturer at the University of Birmingham, told the Daily Mail.

Weaponized pesticides

Tellingly, many nerve agents were first developed as pesticides. Sarin, for example — a deadly chemical warfare agent believed to be responsible for the deaths of hundreds of civilians in Syria — was created as a pesticide by German scientists in 1938. In its liquid and gaseous forms, sarin is colorless, odorless and tasteless, making it nearly impossible to detect until poisoning symptoms have already set in. Depending on the degree of exposure, symptoms from sarin poisoning may take only a few seconds to appear. (Sarin and many other nerve agents are banned by the Chemical Weapons Convention, which more than 190 nations, including Syria, participate in.)

It is unlikely that Skripal and his daughter were poisoned with sarin, a source close to the investigation told the BBC. Investigators also believe that the poison in question was not VX (or "Venomous Agent X") — another deadly nerve agent banned by the Chemical Weapons Convention. VX was used to assassinate Kim Jong-nam, the half brother of North Korean leader Kim Jong-un, at an airport last year.

Investigators believe the nerve agent used against the Skripals was "very rare," the BBC reported, and was likely manufactured in a country with a large infrastructure capable of creating and delivering such deadly man-made toxins. It may take days or weeks before toxicologists can provide an answer. In the meantime, the area where the Skripals were found has since been hosed down, which should help dilute any remnants of the chemical agent, an emergency-medicine doctor told Live Science. Nevertheless, the site remains closed to the public.

Originally published on Live Science.

In the fall of 1925, two medical students in Kirksville, Missouri, received a cadaver and a challenge. Their assignment: to dissect the body's nervous system, beginning at the base of the brain and working downward, leaving the system in one continuous piece.

Over the following year, the students — M.A. Schalck and L.P. Ramsdell — spent 1,500 hours of their lives completing the painstaking dissection. A viral photo posted on Reddit on Jan. 30 shows the extraordinary fruits of their labor, which remain on permanent display at the Museum of Osteopathic Medicine at A.T. Still University (ATSU) in Kirksville.

"Medical students come into the museum and stare at it in amazement," Jason Haxton, director of the museum, told Live Science. "Sometimes, they'll run in after a test to check their work. People familiar with dissection say this is truly a miracle piece." [Image Gallery: The Oddities of Human Anatomy] 

According to Haxton, every student in Schalck and Ramsdell's class at the Kirksville College of Osteopathy & Surgery (an institution founded by Dr. Andrew Taylor Still in 1892, now part of ATSU) was required to dissect a human arm. "These two students' dissections were so detailed, and so much better than any other student's, that they were chosen to dissect an entire body," Haxton said.

Schalck and Ramsdell operated downward from the body's brain stem, exposing the spinal cord and cutting through skin, muscle and protective tissue to clear the maze of nerve fibers within.

"After they cleared each nerve, they rolled them in cotton batting soaked in some kind of preservative," Haxton said. (The exact preservative chemicals used are unknown.) "So, as they worked their way down, there was just a mass of little rolls of cotton."

After 1,500 hours of surgery, Schalck and Ramsdell mounted the dissected nervous system on a slab of shellacked wood. They added hundreds of paper labels to the display and exhibited the finished dissection at medical conferences and museums around the country.

Today, Haxton said, Schalck and Ramsdell's nervous system is one of only four such dissections in the world. (He said he excludes nervous systems exhibited by the traveling exposition Body Worlds, which uses chemicals to help extract the fibers.) In 1936, researchers at ATSU dissected a second nervous system and then donated it to the Smithsonian Institution. A third sample is owned by a medical museum in Thailand, Haxton said, and a fourth is on display at Drexel University in Philadelphia.

"The school anatomist [at Drexel] had a cleaning lady named Harriet," Haxton said. "She donated her body at death, and the anatomist wanted to do something absolutely fantastic. So, in 1888, he dissected her."

As for the person whose body ended up on Schalck and Ramsdell's operating table, nothing is known. Whoever it was likely died in prison or in a poor house, Haxton said, as those were the main state-approved sources of medical cadavers at the time.

Whoever this long-departed Missourian may have been, though, this much is clear: He or she left behind what is now one of the most valuable nervous systems in the world. About 10 years ago, Haxton said, the exhibit was valued at $1 million.

Originally published on Live Science.

A bizarre new species of marine worm lacks a number of internal features common to other animals — including an anus, new research shows.

The strange, pale-orange creature, scientifically known as Xenoturbella japonica, was found on the seafloor of the western Pacific Ocean. A team of scientists from the University of Tsukuba in Japan revealed that the worm lacks certain features common among more complex animals, such as a centralized nervous system, kidneys and an anus. However, the creature does have an oval-shaped mouth, implying that its digestive system has only one opening.

This new species belongs to a group of worms that holds a controversial place in the tree of life, as a sister group of the Bilateria — the group that contains the most-complex animals, including humans. Therefore, the discovery of this new species could shed light on the origin of animals' complex internal body parts, the scientists in the new study said in a statement. [In Photos: Spooky Deep-Sea Creatures]

In the study, the researchers examined two specimens of X. japonica, including a female about 2 inches (5 centimeters) in length and a juvenile about 0.4 inches (1 cm) in length. The scientists used micro-computed tomography (micro-CT) scans to reveal the inner workings of the worm, and its "frontal pore," which traditional methods are unable to capture, according to the statement.

To see where X. japonica fits in the tree of life, the team also extracted DNA from the worm cells' nucleus and mitochondria, the energy powerhouse of the cell, study co-author Hideyuki Miyazawa said in the statement. "Analysis confirmed that X. japonica is distinct from previously described species of Xenoturbella."

The researchers also found DNA contamination from several species of bivalve, which suggests that X. japonica feeds on marine bivalves, much like other marine worms in the genus Xenoturbella do.

"Species within this genus have previously been divided into 'shallow' and 'deep' subgroups, and our results place X. japonica in the 'shallow' subgroup," lead author Hiroaki Nakano said in the statement. "Interestingly, X. japonica shares features with both subgroups, however. Thus, features of this species may be ancestral for this genus, and this new species may be particularly important for unraveling the ancestry of Xenoturbella and the early history of the Bilateria."

Studying marine worms in the genus Xenoturbella has proven to be difficult in the past, because the creatures dwell hundreds or thousands of feet beneath the surface. However, the latest discovery could offer a new solution, the researchers said.

"One habitat where X. japonica was found is easily accessible from a marine station," so the new species could be valuable for researching the evolution of these types of worms, co-author Hisanori Kohtsuka said in the statement.

The findings were published Dec. 18 in the journal BMC Evolutionary Biology.

Original article published on Live Science.

If you get the urge to pee when you're nervous, you're not alone.

It's common to feel the need to void your bladder when you're feeling tense, said Dr. Tom Chi, an associate professor of urology at the University of California, San Francisco.

"When in doubt, just do what your body says, and go to the bathroom — you'll probably be OK," Chi told Live Science. [Why Does Asparagus Make Your Pee Smell Funny?]

In a typical situation, when you're not feeling nervous or anxious, the bladder is relaxed as it fills with urine from the kidneys. In contrast, the bladder's external sphincter is tightly closed to make sure that urine doesn't leak out, Chi said.

A healthy bladder can hold up to 2 cups (16 fluid ounces) of urine. Once the muscular sac is full, "the bladder sends a signal through the spine up to the brain that says, 'OK, I'm full; I got to go,'" Chi said. Once this signal is received and the person is ready, the bladder contracts, and the external sphincter muscle relaxes, letting a stream of pee flow.

Doctors aren't entirely sure why people tend feel the call of nature during times of anxiety, largely because the need to pee is controlled by many factors, including the nerves along the spinal cord, the brain and your emotions. But researchers have two good guesses for why this phenomenon happens, Chi said.

One idea is that when you're anxious or nervous, your body goes into fight-or-flight mode. This tense, adrenaline-filled response may stimulate the need to relieve yourself. The fight-or-flight response may also increase the kidneys' production of urine, Chi said.

The reasons linking this response to the need to void aren't fully understood. But it's thought that "under stress, the [central nervous] system is activated to operate at a higher level of sensitivity, meaning that it takes less to activate the reflex," Dr. Alan Wein, a professor of urology at Penn Medicine at the University of Pennsylvania, told Live Science.

The other idea is that when you're nervous, your muscles tense up, "and one of those muscles may be the bladder," Chi said. "When that happens, it makes you want to pee."

If you're nervous and feel the need to pee but you don't have easy access to a bathroom, Chi recommended distracting yourself or doing meditation exercises to relax your mind and muscles.

Original article on Live Science.

With a nod to the "Voltron" Defender of the Universe" — the animated show in which five lion-shaped robots link up to form a giant machine that fights evil — a team of scientists has created robots that work together and decide which one will lead them.

Typically, if a robot's "brain" (or central processor) gets damaged or destroyed, the machine must take a trip to the great robot repair shop in the sky (or technician's bench).

However, a team led by Marco Dorigo, who heads a robotics lab at the Free University of Brussels, built a robot of sorts that has a fallback, or fallbacks: These robots can link up, react to their environment and delegate authority to a single member of a group. They can add new robots and merge groups, and if the leader of the robots is damaged (or its battery runs out), the other robots can pick a new leader and continue with a task.  [Super-Intelligent Machines: 7 Robotic Futures]

"It's like a bunch of people gathering to build a house," Dorigo told Live Science. "Everyone knows approximately what to do, but if there's no structure, no hierarchy, building a house is difficult." These new robots create their own hierarchies; they choose one to be the leader, which can direct the others.

The robots can also link up so that they can accomplish tasks that they couldn't complete by themselves. The team demonstrated one robot that, in order to lift a brick, had to connect with another robot that had arms.

Robots that work in unison aren't unusual; flying drones can dance together and rebuild their formations when one is missing. The difference is that those drones often operate in a preprogrammed way, using their ability to sense their positions when creating their formations, Dorigo said. Thus, they have a limited ability to adapt, he said.

These Voltron-like robots, on the other hand, can (by linking up) create a kind of nervous system, deciding which one will be the brain (called the parent by the researchers) and which will be the limb (called the child). This arrangement allows the group to adapt to new conditions. In one video, one robot stops functioning and the others choose a new leader, which will be the brains of the system. (The robots know their leader has stopped working because it doesn't acknowledge signals from the others.)

This brain-children setup works because the robots all have an internal map of the others that are connected to them, and that map looks like a hierarchical tree, said Nithin Mathews, lead author of the paper describing the work. When the lead robot stops working, the others can see where in the tree they are; those closer to the "root" are more likely to be chosen as leads.

It can also be environment-dependent. For example, if a bunch of robots were near some resource they needed, the closest one to that resource would take over as the head.

Further, when two groups of robots join together, the leader of the first group can transfer its internal map of the other robots to the leader of the second group, giving up the leadership position and becoming part of the now-larger group.

Mathews said the architecture was in part inspired by slime molds, which are simple organisms that join together to behave as a kind of super-organism. The robots work in a similar fashion, he said. "Slime mold can come together as single body, but the nervous system is missing," Mathews said. "Higher-order animals have nervous system with single brain unit. We thought, 'Lets bring these worlds together.'"

While the robots used so far are very simple — they are just wheeled carts smaller than a Roomba vacuum — the achievement suggests that robots can be trained to adapt as a group to new environments, Mathews said. Further, they can even be made of many parts; imagine a robot that is using an arm (which itself is an autonomous robot) to pick up something, and the arm gets damaged. That robot could go seek a new limb.

The big obstacle, Mathews said, is that there's no standard for robots to interact. The team had to invent the language the robots used to speak to each other. "I think there will need to be a lot of intermediate steps" before such robots are common in industry, he said.

The study is detailed in the Sept 12 issue of the journal Nature Communications.

Originally published on Live Science.

Humans spend nearly a third of their lives asleep. Going without sleep will literally make you psychotic and, eventually, kill you. It's clear that shut-eye is crucial to the body's ability to function.

But no one knows what sleep actually does.

"It's sort of embarrassing," said Dr. Michael Halassa, a neuroscientist at New York University. "It's obvious why we need to eat, for example, and reproduce … but it's not clear why we need to sleep at all." [5 Surprising Sleep Discoveries]

We're vulnerable when we're asleep, so whatever sleep does, it must be worth the risk of the brain taking itself mostly offline. There are a few theories about why we sleep, and although none of them are totally solid, a few try to explain what happens each night, pulling in research on topics ranging from cellular processes to cognition. Researchers say it does seem clear that sleep is key to the brain's ability to reorganize itself — a feature called plasticity.

Sleep stages

It's not hard to prove that sleep is important. Rats totally deprived of sleep die within two or three weeks, according to research by the pioneering University of Chicago sleep scientist Allan Rechtschaffen. No one has done similar experiments on humans, for obvious reasons, but a 2014 study published in The Journal of Neuroscience found that a mere 24 hours of sleep deprivation caused healthy people to have hallucinations and other schizophrenia-like symptoms.

One reason it is difficult to get a handle on why we sleep is that sleep is actually pretty difficult to isolate and study. Sleep-deprivation studies are the most common way to study sleep, said Marcos Frank, a neuroscientist at the University of Washington, but depriving an animal of sleep disrupts many of its biological systems. It's hard to tell which outcomes are directly attributable to sleep deprivation rather than, say, stress.

Another reason sleep is hard to understand is that the brain may be doing two different things during the two major stages of sleep. As the night wears on, sleepers cycle through non-rapid eye movement (non-REM) and rapid-eye-movement (REM) sleep. Non-REM sleep is marked by slow brain waves called theta and delta waves. In contrast, the brain's electrical activity during REM sleep looks much like it does when a person is awake, but the muscles of the body are paralyzed. (If you've ever experienced sleep paralysis, it's because you woke from REM sleep before this paralysis ended.)

Studies have found differences in the biology of the brain during these different stages. For example, during non-REM sleep, the body releases growth hormone, according to a 2006 review of the biology of sleep published by Frank in the journal Reviews in the Neurosciences. Also during non-REM sleep, the synthesis of some brain proteins increases, and some genes involved in protein synthesis become more active, the review found. During REM sleep, in contrast, there does not appear to be any increase in this sort of protein-producing activity.

What do we know about sleep?

One conclusion that has emerged from sleep research is that sleep does appear to be largely a brain-focused phenomenon, Frank said. Although sleep deprivation affects the immune system and alters hormone levels in the body, its most consistent impacts across animals are in the brain. [10 Things You Didn't Know About the Brain]

"The central nervous system is always impacted by sleep," Frank said. "There may have been other things that evolution added onto the primary function of sleep, but the primary function of sleep probably has something to do with the brain."

There is some evidence, in fact, that sleep is just something that neurons do when they're joined in a network. Even neuron networks grown in lab dishes show stages of activity and inactivity that sort of resemble waking and sleeping, Frank said. That could mean sleep arises naturally when single neurons begin to work together.

This could explain why even the simplest organisms show sleep-like behaviors. Even Caenorhabditis elegans, a tiny worm with only 302 neurons, cycles through quiet, lethargic periods that look like sleep. Perhaps the first simple nervous systems to evolve exhibited these quiet periods, Frank said, and as brains got larger and more complex, the state of inactivity also had to get more complicated.

"It would be very disadvantageous to have a complex brain like ours where different parts are falling in and out of sleep, so you need to have some way to orchestrate this," he said.

What happens during sleep?

But the idea that sleep is a natural property of neuron networks doesn't really explain what's going on during sleep. On that front, scientists have a number of theories. One is that sleep restores the brain's energy, according to a 2016 review in the journal Sleep Medicine Reviews. During non-REM sleep, the brain consumes only about half the glucose as it does when a person is awake. (Glucose is the sugar that cells burn up to release energy.)

But if the idea that sleep restores brain energy is true, the relationship between sleep and the brain's energy usage is not straightforward. For example, during sleep deprivation, the brain's breakdown of an energy source called glycogen increases in some parts of the brain but decreases in others. More research is needed to understand this link. [The 7 Biggest Mysteries of the Human Body]

Another idea is that sleep might enable the brain to clear out toxic products produced when we're awake. The brain is a huge consumer of energy, which means it also produces much waste. Some recent research suggests that sleep is a time when the brain sweeps itself clean, Frank said, but those results need to be replicated.

"It might be something that kind of happens with sleep," Frank said, "but it may not be the most important thing sleep is doing."  

Perhaps the most promising theory of sleep so far is that it plays a major role in the brain's connectivity and plasticity. Plasticity is involved in learning and memory. Although it's unclear exactly how, plenty of evidence suggests that losing sleep can cause problems with memory, particularly working memory, the process that allows people to hold information in an easily accessible way while working out a problem. People who are sleep-deprived also struggle with choosing what to pay attentionto and regulating their emotions.

One way sleep may affect the brain's plasticity is through its effects on the synapses, or connections between neurons. Research has shown that when animals learn a new task, their neurons seem to strengthen the synaptic connections involved in learning that task during the next sleep cycle, according to the Sleep Medicine Reviews paper. In experiments where researchers put a patch over one of an animal's eyes, the brain circuits associated with visual information from that eye weakened within hours, according to research by the University of Surrey's Julie Seibt and colleagues. REM sleep, however, strengthened the circuits involving the other eye, suggesting that the brain uses sleep to adjust to changing inputs. [7 Weird Facts About Balance]  

"It could still mean there is something really basic and central at the heart of [sleep], something basic that brain cells have to do, and one outcome is the plastic change," Frank said.

In the future, a better understanding of sleep may come from research on cells called glia cells, Frank said. These brain cells, whose name literally means "glue," were once thought to be largely inert but have been recently discovered to have a range of functions. Glia cells outnumber neurons by up to three to one, Frank said. Glia cells may control the flow of cerebrospinal fluid throughout the brain, which could result in clearing out metabolic waste during sleep, for example.

"It could be that the mystery of sleep could be solved by understanding what these very specialized glia cells are doing," Frank said.

Original article on Live Science. 

Parkinson's disease, which involves the malfunction and death of nerve cells in the brain, may originate in the gut, new research suggests, adding to a growing body of evidence supporting the idea.

The new study shows that a protein in nerve cells that becomes corrupted and then forms clumps in the brains of people with Parkinson's can also be found in cells that line the small intestine. The research was done in both mice and human cells.

The finding supports the idea that this protein first becomes altered in the gut and then travels to the brain, where it causes the symptoms of Parkinson's disease.

Parkinson's disease is a progressive movement disorder, affecting as many as 1 million people in the United States and 7 million to 10 million people worldwide, according to the Parkinson's Disease Foundation.

The protein, called alpha-synuclein, is abundant in the brain. And in healthy nerve cells, it dissolves in the fluid within the cell. But in Parkinson's patients, alpha-synuclein folds abnormally. The misfolded protein can then spread through the nervous system to the brain as a prion, or infectious protein. In the brain, the misfolded protein molecules stick to each other and clump up, damaging neurons. [6 Foods That Are Good for Your Brain]

In 2005, researchers reported that people with Parkinson's disease who had these clumps in their brains also had the clumps in their guts. Other research published this year looked at people who had ulcers and who underwent a surgery that removed the base of the vagus nerve, which connects the brain stem to the abdomen. These patients had a 40 percent lower risk of developing Parkinson's later in life compared with people who didn't have their vagus nerve removed.

Both findings suggested the prion may originate in the gut.

But one puzzle remained: how the proteins that became altered in the gut could spread to the brain. The protein had been found in the lumen, or the space inside the gastrointestinal tract, but "nerves are not open to the lumen," said gastroenterologist Dr. Rodger Liddle, senior author of the new paper, appearing today (June 15) in the journal JCI Insight, and professor of medicine at Duke University in North Carolina.  

A key clue to how the protein may move from the lumen into nerve cells came in 2015. Liddle's team discovered cells in the lining of the small intestine that "acted a lot like nerve cells," Liddle said. The cells were endocrine cells, meaning they produce hormones, but they contained neurotransmitters and other proteins normally found in neurons. These cells even appeared to branch out in a similar way that neurons do, to communicate.

When placed near neurons, these endocrine cells behaved a lot like neurons – the endocrine cells moved toward the neurons, and fibers sprouted between the cells, connecting them, Liddle said. The process was captured in a time-lapse video featured in the 2015 study in the Journal of Clinical Investigation.

"It was only afterwards that we started putting these things together — these cells have a lot of nerve-like properties, [so] let's see if they also contain alpha-synuclein. And if they do, maybe they could be the source of Parkinson's disease," Liddle told Live Science. [10 Things You Didn't Know About the Brain]

Now that Liddle's team has shown that the endocrine cells do, in fact, contain the alpha-synuclein protein, the researchers want to establish that the endocrine cells of Parkinson's patients carry the malformed version of the protein, Liddle said.

If they can establish that, Liddle said, they can envision how the corrupted proteins causing Parkinson's disease could spread from the gut lining to the brain, possibly via the vagus nerve.

Previous research has shown that people exposed to certain pesticides and bacteria are more likely to get Parkinson's. Liddle said that one possibility is that these agents may affect the nerve-like endocrine cells in the gut, altering the structure of the alpha-synuclein protein inside the gut cells.

"Maybe it's bacteria, maybe a toxin that people ingest. Maybe they affect the endocrine cell and that corrupts the alpha-synuclein protein, and that spreads from the cell to the vagus nerve to the brain," Liddle told Live Science.

For now, many "maybe's" remain. But if further research supports the hypothesis, it could point the way to new ways to diagnose Parkinson's disease early on, as well as to new approaches to treatment, Liddle said.

"It's possible that if it starts in the gut, then you could create treatments that prevent abnormal alpha-synuclein formation in these cells," Liddle said. "It's possible you could develop dietary ways of treating those cells because those cells are lining the intestine. At this point, it's difficult to imagine, but we will see."

Originally published on Live Science.