Cellular origins of auditory event-related potential deficits in Rett syndrome
D Goffin, ES Brodkin, JA Blendy, SJ Siegel… - Nature neuroscience, 2014 - nature.com
D Goffin, ES Brodkin, JA Blendy, SJ Siegel, Z Zhou
Nature neuroscience, 2014•nature.comDysfunction in sensory information processing is a hallmark of many neurological disorders,
including autism spectrum disorders, schizophrenia and Rett syndrome (RTT). Using mouse
models of RTT, a monogenic disorder caused by mutations in MECP2, we found that the
large-scale loss of MeCP2 from forebrain GABAergic interneurons led to deficits in auditory
event-related potentials and seizure manifestation, whereas the restoration of MeCP2 in
specific classes of interneurons ameliorated these deficits.
including autism spectrum disorders, schizophrenia and Rett syndrome (RTT). Using mouse
models of RTT, a monogenic disorder caused by mutations in MECP2, we found that the
large-scale loss of MeCP2 from forebrain GABAergic interneurons led to deficits in auditory
event-related potentials and seizure manifestation, whereas the restoration of MeCP2 in
specific classes of interneurons ameliorated these deficits.
Abstract
Dysfunction in sensory information processing is a hallmark of many neurological disorders, including autism spectrum disorders, schizophrenia and Rett syndrome (RTT). Using mouse models of RTT, a monogenic disorder caused by mutations in MECP2, we found that the large-scale loss of MeCP2 from forebrain GABAergic interneurons led to deficits in auditory event-related potentials and seizure manifestation, whereas the restoration of MeCP2 in specific classes of interneurons ameliorated these deficits.
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