Hundreds of millions of people worldwide suffer from a vision condition called amblyopia, or lazy eye, with imbalanced vision in their two eyes. Unless this disabling condition is caught and treated at a young age, it's rare for children to regain full vision, because the brain learns to turn off the input from the "lazy" eye. Amblyopia is one striking example of how the brain is modified by experience

Research of professor Mark Bear, a neuroscientist at MIT's Picower Institute for Learning and Memory from Massachusetts Institute of Technology focuses on this phenomenon of brain plasticity, with particular attention to the synapses that connect neurons in the brain.

Studies have led to a potential treatment for amblyopia that works by temporarily anesthetizing the "good" eye. After successful experiments in smaller animals, the method is being tested in non-human primates, and researchers hope to move ahead into clinical trials.

There is the challenge of seeing one world through two eyes. To avoid seeing double, information from the two retinas must be mapped with extreme precision onto common targets in the brain. But we're not born with this ability; it depends on high-quality visual experience during infancy and early childhood. This need for the brain to learn to see fully was demonstrated decades ago, in experiments with young animals with a patch placed over one eye. When the patch was removed, researchers discovered a severe visual impairment through the eye that had been patched. The retina was fine.. The problem was that it had been mis-wired in the brain, so that these connections didn't mature normally.

Researchers trace the whole path that goes from poor-quality visual experience to poor quality-of-vision and visual impairment in the brain. Research has demonstrated that the condition is triggered by replacing well-correlated activity in the retinas with retinal noise. That type of activity weakly activates a particular neurotransmitter receptor in the brain called an NMDA receptor, which triggers the modification of synapses that causes those synapses to get weaker.

These findings have practical implications for the vast number of children born with amblyopia, usually due to one of three causes. Their eyes may be cross-eyed, or they may be born with a cataract in one eye, or the two eyes refract (focus) differently so that they only view the world crisply through one eye or the other. All of these mishaps disrupt the wiring of the brain, resulting in poor visual acuity in one eye and loss of binocular vision.

The current medical treatment is simply to put a patch over the good eye, to try to force relearning of vision through the weak eye. This procedure can work but is rarely completely successful. And it must begin early.

Amblyopia is particularly devastating for people who later lose use of their good eye. But in a surprising number of cases, the amblyopic eye then does recover some vision, even in adults. That means there is plasticity in the adult brain, which is good.

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