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When one eye is deprived of vision early in life, it can lead to amblyopia, a condition more commonly known as lazy eye. This happens because a lack of input disrupts synapse formation in the brain’s primary visual cortex, weakening vision in that eye.
In 2016, researchers found that temporarily numbing both retinas could reverse vision loss from amblyopia, while a follow-up study in 2021 showed that numbing only the non-amblyopic eye could also improve vision in the weaker eye. This method is like the treatment used for children, which involves patching the healthy eye. These findings have been verified in adult animals of different species.
A new mouse study from neuroscientists at MIT’s Picower Institute shows that briefly and reversibly anesthetizing the retina of the amblyopic eye for just a few days can restore the brain’s visual responses to that eye, even in adults. The results strengthen the idea that temporarily numbing a retina could help rebuild the weakened neural connections in an amblyopic eye.
“The amblyopic eye, which is not doing much, could be inactivated and ‘brought back to life’ instead,” says Picower Professor Mark Bear. “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.”
The team was particularly interested in how this retinal inactivation produces its effects. One of the clues to a possible answer lay in an old research finding from 2008. Connecting the retina to the visual cortex is a structure called the lateral geniculate nucleus (LGN). When input from the retina was blocked to neurons in the LGN the prior research saw those LGN neurons fire bursts of activity to downstream neurons in the visual cortex.
Researchers wanted to find out whether this burst-like activity occurred only in LGN neurons that had lost input, or also in neurons receiving signals from the eye that could still see. After some clever experiments the researchers discovered that this burst activity was indeed the way the brain seemed to recover vision in a damaged eye.
The researchers are still left with some interesting unanswered questions. It seems clear that temporarily anesthetizing one eye does seem to reset the way the brain engages these LGN neurons but exactly why this is happening is still unclear.
“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 researchers conclude in the new study.
The findings are published in Cell Reports.
Source: MIT
