Modulation of prefrontal cortex excitation/inhibition balance rescues social behavior in CNTNAP2-deficient mice

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Science Translational Medicine  02 Aug 2017:
Vol. 9, Issue 401, eaah6733
DOI: 10.1126/scitranslmed.aah6733

Social interactions light up

Neurophysiological phenomena that underlie the symptoms of autism remain unclear. Genetics-based mouse models of autism have suggested that there is an increase in the neuronal excitation/inhibition (E:I) balance. An optogenetically driven increase in this E:I balance leads to social deficits in mice. Using mice lacking CNTNAP2, a gene known to be associated with autism in humans, Selimbeyoglu and colleagues now show that real-time optogenetic modulation of the E:I balance rescued social behavior deficits and hyperactivity in these animals. This study highlights the potential for modulating neural circuits in the brain as a strategy for treating autism.

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