Anesthetising Amblyopic Eye to Reboot Vision

In amblyopia, impaired vision in one eye during development causes neural connections in the brain’s visual system to shift toward supporting the other eye, leaving the amblyopic eye less capable, even after the original impairment is corrected. Current interventions are only effective during infancy and early childhood, while the neural connections are still being formed.

Neuroscientists at The Picower Institute for Learning and Memory at MIT have been experimenting with the concept of rebooting vision via anaesthesia in animal models for some years.

In a 2016 study with collaborators at Dalhousie University, they showed that temporarily anaesthetising both retinas could restore vision loss in amblyopia. Then, five years later, they published a study showing that anaesthetising just the non-amblyopic eye produced visual recovery for the amblyopic eye – an approach analogous to the childhood treatment of patching the unimpaired eye. Those 2021 findings have now been replicated in adults of multiple species.

Now, their new evidence on how inactivation works suggests that the proposed treatment also could be effective when applied directly to the amblyopic eye. However, a key next step will be to again show that it works in additional species and, ultimately, people.

“If it does, it’s a pretty substantial step forward, because it would be reassuring to know that vision in the good eye would not have to be interrupted by treatment,” said Dr Bear, a faculty member in MIT’s Department of Brain and Cognitive Sciences and co-author of the study. “The amblyopic eye, which is not doing much, could be inactivated and ‘brought back to life’ instead. Still, I think that especially with any invasive treatment, it’s extremely important to confirm the results in higher species with visual systems closer to our own.”

Madison Echavarri-Leet, whose doctoral thesis included this research, is the lead author of the study, which also demonstrated the underlying process in the brain that makes the potential treatment work.

A Beneficial Burst

Over the decades, Dr Bear’s lab has considered multiple hypotheses to explain how retinal inactivation reboots vision. One of these was that the lateral geniculate nucleus (LGN) relays information from the eyes to the visual cortex, where vision is processed. Back in 2008, they had found that blocking inputs from a retina to neurons in the LGN caused those neurons to fire synchronous ‘bursts’ of electrical signals to downstream neurons in the visual cortex. Similar patterns of activity occur in the visual system before birth and guide early synaptic development.

The new study tested whether those bursts might have a role in potential amblyopia treatments being reported. To get started, the team used a single injection of tetrodotoxin (TTX) to anesthetise retinas in the laboratory animals. They found that the bursting occurred not only in LGN neurons that received input from the anesthetised eye, but also in LGN neurons that received input from the unaffected eye.

From there, they showed that the bursting response depended on a particular ‘T-type’ channel for calcium in the LGN neurons. This gave the scientists a way to turn it off, enabling them to test whether doing so prevented TTX from having a therapeutic effect in mice with amblyopia.

Sure enough, when the researchers genetically knocked out the channels and disrupted the bursting, they found that anesthetising the non-amblyopic eye could no longer help amblyopic mice. That showed that the bursting is necessary for the treatment to work.

Aiding Amblyopia

Given their finding that bursting occurs when either retina is anesthetised, the scientists hypothesised it might be enough to just do it in the amblyopic eye. To test this, they ran an experiment in which some mice modelling amblyopia received TTX in their amblyopic eye and some did not. The injection took the retina offline for two days. A week later, the scientists measured activity in neurons in the visual cortex to calculate a ratio of input from each eye. They found that the ratio was much more even in mice that received the treatment versus those left untreated, indicating that after the amblyopic eye was anaesthetised, its input in the brain rose to be at parity with input from the non-amblyopic one.

Further testing is needed, Dr Bear said, but the team wrote in the study that the results were encouraging.

“We are cautiously optimistic that these findings may lead to a new treatment approach for human amblyopia, particularly given the discovery that silencing the amblyopic eye is effective,” the scientists wrote.

References

1. Orenstein D. MIT study shows how vision can be rebooted in adults with amblyopia. MIT News. Available at mit.edu/2025/how-vision-can-be-rebooted-in-adults-with-amblyopia-lazy-eye-1210 [accessed Jan 2026]
2. Echavarri-Leet, Madison et al. Temporary retinal inactivation reverses effects of long-term monocular deprivation in visual cortex by induction of burst mode firing in the thalamus. Cell Reports, Volume 44, Issue 11, 116566