Bear’s team, which has been studying amblyopia for decades, had previously shown that this effect could be achieved by anesthetizing both eyes or the non-­amblyopic eye, analogous to having a child wear a patch over the healthy eye to strengthen the “lazy” one. 

The new study delved into the mechanism behind this effect by pursuing an earlier observation: that blocking the retina from sending signals to neurons in the part of the brain that relays information from the eyes to the visual cortex caused those neurons to fire “bursts” of electrical pulses. Similar patterns of activity occur in the visual system before birth and guide early synaptic development.

The experiments confirmed that the bursting is necessary for the treatment to work—and, crucially, that it occurs when either retina is targeted. After some mice modeling amblyopia had the affected eye anesthetized for two days, the researchers measured activity in the visual cortex to calculate a ratio of inputs from the two eyes. This ratio was much more even in the treated mice, indicating that the amblyopic eye was communicating with the brain about as well as the other one.

A key next step will be to show that this approach works in other animals 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,” says Bear. “The amblyopic eye, which is not doing much, could be inactivated and ‘brought back to life’ instead.”