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Surprisingly, despite the diversity of these features, we have found that deleting Mecp2 only from GABAergic inhibitory neurons in mice replicates most of this phenotype. Here we show that genetically restoring Mecp2 expression only in GABAergic neurons of male Mecp2 null mice enhanced inhibitory signaling, extended lifespan, and rescued ataxia, apraxia, and social abnormalities but did not rescue tremor or anxiety. Female Mecp2+\/- mice showed a less dramatic but still substantial rescue. These findings highlight the critical regulatory role of GABAergic neurons in certain behaviors and suggest that modulating the excitatory\/inhibitory balance through GABAergic neurons could prove a viable therapeutic option in Rett syndrome.<\/jats:p>","DOI":"10.7554\/elife.14198","type":"journal-article","created":{"date-parts":[[2016,6,21]],"date-time":"2016-06-21T07:59:58Z","timestamp":1466495998000},"source":"Crossref","is-referenced-by-count":117,"title":["Restoration of Mecp2 expression in GABAergic neurons is sufficient to rescue multiple disease features in a mouse model of Rett syndrome"],"prefix":"10.7554","volume":"5","author":[{"given":"Kerstin","family":"Ure","sequence":"first","affiliation":[{"name":"Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, United States"},{"name":"Jan and Dan Duncan Neurological Research Institute, Texas Children's Hospital, Houston, United 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