Injecting anesthetic into a 'lazy eye' may correct it, early study suggests

Researchers think they may have found a way to reverse "lazy eye," even in adults who've typically had the condition since childhood.

The technique has so far been tested only in animals, though, so it needs further study before it can be used in human patients.

A lazy eye, or amblyopia, develops when the brain favors one eye over the other in early childhood, causing vision in the less-favored eye to decline. The standard treatment involves placing a patch over the stronger eye to force the brain to rely on the weaker one. However, this method is effective only during infancy and early childhood, when the neural connections that regulate vision are still being formed.

Now, a mouse study published Nov. 25 in the journal Cell Reports introduces a method for temporarily shutting down the weak eye, which can lead to recovery from amblyopia, even after long-term vision issues. "Rebooting" the lazy eye seems to come from a burst of activity in neurons that pass visual signals from the retina to the visual cortex, a hub for processing visual information in the brain.

"The finding that inactivation of the amblyopic eye enables vision recovery in a mouse model of amblyopia is encouraging," said Ben Thompson, a professor and the director of the School of Optometry and Vision Science at the University of Waterloo in Canada, who was not involved in the study.

But more research is needed to see whether the method will be safe and effective in humans, too, Thompson told Live Science in an email.

Dr. Dennis Levi, a professor of optometry and vision science at the University of California, Berkeley who was not involved in the study, was also cautiously optimistic about the findings. Historically, scientists have tried various methods of reversing lazy eye in mice, but they "failed to produce significant improvements in humans with amblyopia," he told Live Science in an email. But this new technique seems to hold promise.

So, how might temporarily shutting down the weak eye help to restore its vision?

Earlier work from MIT neuroscientist Mark Bear and colleagues showed that anesthetizing the non-lazy eye triggered visual recovery in the lazy eye in older animals, including cats and mice. Similar results have been found in monkeys, which may spell good news for humans, Levi noted.

In the new study, the team hypothesized that blocking input from one retina causes neurons to fire in synchronized bursts in the thalamus, a part of the brain that handles incoming sensory information. Specifically, these bursts are seen in the lateral geniculate nucleus (LGN), part of the brain that relays information from the eyes to the visual cortex.

Similar bursts happen in the LGN before birth and help the visual system develop in the womb. That led the team to wonder whether re-creating this early activity pattern could help treat amblyopia.

They tried injecting a local anesthetic called tetrodotoxin (TTX) into the retinas of mice and then monitored the rodents' LGN neurons. TTX is a neurotoxin found in animals like pufferfish, but it also has potential therapeutic uses, including anesthesia and the treatment of severe pain. Research into these uses in humans is ongoing, but in the context of this study, TTX was useful for rebooting the retinas of mice.

The researchers found that shutting down either eye triggered the same burst pattern in the LGN. In a second experiment, they genetically modified the mice so their LGN neurons couldn't produce this burst firing. The activity stopped, and the anesthetic treatment no longer improved amblyopia. That showed that the bursts themselves were crucial for recovery.

Next, the team tested whether they could treat amblyopia by inactivating only the weak eye. They ran an experiment in which some mice with amblyopia got an injection in their weak eye while others did not. The injection stopped the retina from sending signals for about two days.

A week after the injection, the scientists measured how much each eye influenced activity in the visual cortex and found that the treated mice had a much more balanced input from both eyes than the untreated mice did. This showed that shutting down the weak eye for a short time helped it "catch up" with the other eye.

Thompson said this result is encouraging "because the fellow eye does not have to be exposed to any risks of the treatment." But he emphasized that "more work is needed to assess whether tetrodotoxin will be safe and effective in humans."

Previous studies suggest that the effects of TTX on amblyopia generalize to cats and monkeys, raising hope that the approach may one day help humans as well.

The discovery that burst firing can help boost the brain's ability to rewire and form new networks is "extremely interesting," Thompson said. Noninvasive tools used to stimulate the brain might eventually be harnessed to trigger similar neural responses, without the need for TTX injections, he added.