Beer’s team, which has been studying amblyopia for decades, previously showed that this effect could be achieved by anesthetizing both eyes or the non-amblyopic eye, such as a child wearing a patch over the healthy eye to strengthen the “lazy” eye.
New Study We delved deeper into the mechanism behind this effect by following up on an earlier observation: blocking the retina from sending signals to neurons in the part of the brain that relays information from the eyes to the visual cortex, causing a “burst” of electrical pulses in those neurons. Similar patterns of activity occur in the visual system before birth and guide early synaptic development.
The experiments confirmed that bursting is necessary for the treatment to be effective – and, importantly, it occurs when the retina is targeted. After anesthetizing the affected eye of some mice modeling amblyopia for two days, the researchers measured activity in the visual cortex to calculate the ratio of input from both eyes. This ratio was also much higher in treated mice, indicating that the amblyopic eye was communicating with the brain as well as the other one.
The next important step will be to show that this approach also works in other animals and eventually people.
“If that happens, it would be a huge step forward, because it would be reassuring to know that vision in the good eye won’t have to be disrupted because of the treatment,” says Baer. “The amblyopic eye, which isn’t doing much, can be deactivated and brought ‘back to life’ instead.”
