A new research has identified an essential circuit within the developing visual system that helps dictate how the eyes connect to the brain, and has implications for treating amblyopia.

Amblyopia is a vision disorder that occurs when the brain ignores one eye in favour of the other.

Fifty years of research on it has even led to a general theory of plasticity called the sliding threshold model. The new study tested a fundamental piece of a model that at first seems at odds with ocular dominance.

Working with the lab of Xiangmin Xu, Ph.D., at the University of California, Irvine, Dr. Joshua Trachtenberg and his team at UCLA investigated this problem in mice. To induce changes in ocular dominance, they temporarily patched one eye in young mice. After 24 hours, they removed the patch and recorded how the firing rate of binocular zone cells changed in response to vision through each eye.

They found that the cells` firing rates immediately dropped by half when vision was restricted to one eye, as expected. But over the next 24 hours, the cells responding to either eye-even the eye that had been temporarily patched-increased their firing rate back to the normal range.

The team`s next goal was to explain the increased firing rate. "Since the signals from the patched eye to the binocular zone are reduced, we wanted to know what drives the increase," Dr. Trachtenberg said.

First, they investigated the possibility that the binocular zone cells were getting more stimulation from other parts of the brain, but that wasn`t the case. Instead, the key turned out to be a brain circuit that normally inhibits the cells. When vision through one eye is impaired, the inhibition from that circuit gets weaker. This loss of inhibition restores the cells` firing rate to the range where their connections can be remodeled.

By manipulating this circuit, the researchers were able to prevent ocular dominance in young mice and induce it in older mice that were already beyond the critical period.

According to Dr. Trachtenberg, if this circuit could be controlled in the human brain-for example, with a drug or with implants of the kind sometimes used to treat Parkinson`s-it would open the door to correcting amblyopia years later than is currently possible.

The study was published in journal Nature.