A study by Stanford University investigators suggests that key features of autism reflect an imbalance in signaling from excitatory and inhibitory neurons in a portion of the forebrain, and that reversing the imbalance could alleviate some of its hallmark symptoms. In a series of experiments conducted on a mouse model of the disorder, the scientists showed that reducing the ratio of excitatory to inhibitory signaling countered hyperactivity and deficits in social ability, two classic symptoms of autism in humans. The study was published in the August 2, 2017 issue of Science Translational Medicine. Dr. Karl Deisseroth, Professor of Bioengineering and of Psychiatry and Behavioral Sciences, is the study's senior author. The lead author is former graduate student Aslihan Selimbeyoglu, PhD. The article is titled “Modulation of Prefrontal Cortex Excitation/Inhibition Balance Rescues Social Behavior In CNTNAP2-Deficient Mice.” In 2011, Dr. Deisseroth's group published a study in Nature showing that autism-like behavioral deficits could be induced in ordinary mice by elevating the ratio of excitatory to inhibitory neuronal firing patterns in the mice's medial prefrontal cortex. The new study shows that decreasing that ratio restores normal behavior patterns in a strain of lab mice bioengineered to mimic human autism. These mice carry a mutation equivalent to a corresponding mutation in humans that is associated with autism spectrum disorder. For reasons that are not understood, the incidence of autism spectrum disorder has increased steadily in recent years, said Dr. Deisseroth, a practicing psychiatrist.
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