Nature Neurosci. doi:10.1038/nn.2327 (2009)

Angelman syndrome is a form of mental retardation caused by mutations in the gene UBE3A. Scientists have discovered a role for the Ube3A protein that might explain the learning deficits associated with the disorder.

Benjamin Philpot of the University of North Carolina at Chapel Hill, Michael Ehlers at Duke University in Durham, North Carolina, and their colleagues focused on the mouse visual cortex. They found that, unlike normal mice, when mice lacking Ube3A were exposed to light, they lost synaptic plasticity — the learning-associated ability to change the strength of signals sent between brain cells — in this area. But the Ube3A-deficient mice recovered plasticity when deprived of visual stimuli, suggesting that Ube3A may help to maintain experience-dependent plasticity during periods of high brain activity.