Abstract

Dysfunction in sensory information processing is a hallmark of many neurological disorders including autism spectrum disorders (ASDs), schizophrenia and Rett syndrome (RTT)1. Using mouse models of RTT, a monogenic disorder caused by mutations in MECP22, we demonstrate that the large scale loss of MeCP2 from forebrain GABAergic interneurons leads to deficits in auditory event-related potentials (ERPs) and seizure manifestation; but the restoration of MeCP2 in specific classes of interneurons ameliorates these deficits.

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