Injecting anesthetic drugs may correct ‘lazy eye’, early research suggests

Researchers think they may have found a way to improve “lazy eyes” even in adults who have been suffering from the condition since childhood.

However, this technology has so far only been tested in animals and requires further research before it can be used in human patients.

Lazy eye, or amblyopia, develops in early childhood when the brain prioritizes one eye over the other, resulting in decreased vision in the non-preferred eye. The standard treatment involves patching the stronger eye and making the brain rely on the weaker eye. However, this method only works during infancy and early childhood, when the neural connections that control vision are still forming.

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Now, a mouse study published Nov. 25 in the journal Cell Reports describes a way to temporarily block out weakened eyes, which could lead to recovery from amblyopia even after long-term vision problems. The lazy eye’s “reboot” appears to be caused by a burst of activity in neurons that transmit visual signals from the retina to the visual cortex, the brain’s hub for visual information processing.

“The finding that inactivation of the amblyopic eye allows restoration of vision in a mouse model of amblyopia is encouraging,” said Ben Thompson, professor and chair of the Department of Optometry and Visual Sciences at the University of Waterloo in Canada, who was not involved in the study.

But more research is needed to see if the method is safe and effective in humans, Thompson told Live Science via 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 ways to improve amblyopia in mice, but “none of them have been able to produce significant improvements in humans with amblyopia,” he told Live Science in an email. But this new technology seems promising.

So, wouldn’t temporarily shutting down a weakened eye restore vision?

Previous research by Massachusetts Institute of Technology neuroscientist Mark Baer and colleagues showed that anesthetizing the non-lazy eye caused visual recovery in the lazy eye in older animals such as cats and mice. Similar results have been found in monkeys, which could be good news for humans, Levi noted.

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

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A similar burst occurs in the LGN prenatally to aid in the development of the visual system in utero. Therefore, the research team thought that recreating this early activity pattern might be useful in treating amblyopia.

They injected a local anesthetic called tetrodotoxin (TTX) into the retinas of mice and attempted to monitor LGN neurons in the rodents. TTX is a neurotoxin found in animals such as puffer fish, but it also has potential therapeutic uses such as anesthesia and the treatment of severe pain. Research into their use in humans is ongoing, but in the context of this study, TTX helped reboot the retinas of mice.

The researchers found that shutting down either eye triggered the same burst pattern in the LGN. In the second experiment, mice were genetically modified so that LGN neurons could not generate this burst of firing. Activity ceased and anesthetic treatment no longer improved amblyopia. This showed that the burst itself is important for recovery.

The team then tested whether amblyopia could be treated by inactivating just the weaker eye. They conducted an experiment in which some mice with amblyopia were injected into their weakened eyes, while others were not. With this injection, the retina stopped sending signals for about two days.

A week after the injection, the scientists measured how much each eye affected activity in the visual cortex and found that treated mice had much more balanced input from both eyes than untreated mice. This showed that closing the weaker eye for a short period of time helps the other eye to “catch up.”

Thompson said the results were encouraging “because the other eye does not have to be at risk for treatment.” But he stressed that “further research is needed to assess whether tetrodotoxin is safe and effective for humans.”

Previous studies have suggested that the effects of TTX on amblyopia are similar to cats and monkeys, raising hopes that this approach may one day be useful for humans as well.

The finding that burst firing helps rewire the brain and increase its ability to form new networks is “very interesting,” Thompson said. He added that non-invasive tools used to stimulate the brain could eventually be harnessed to elicit similar neural responses without the need for TTX injections.