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Earlier studies using human induced pluripotent stem cells (iPSCs) have produced mixed results regarding the importance of Nav1.1 in human inhibitory versus excitatory neurons. We studied a Nav1.1 mutation (p.S1328P) identified in a pair of twins with Dravet Syndrome and generated iPSC-derived neurons from these patients. Characterization of the mutant channel revealed a decrease in current amplitude and hypersensitivity to steady-state inactivation. We then differentiated Dravet-Syndrome and control iPSCs into telencephalic excitatory neurons or medial ganglionic eminence (MGE)-like inhibitory neurons. Dravet inhibitory neurons showed deficits in sodium currents and action potential firing, which were rescued by a Nav1.1 transgene, whereas Dravet excitatory neurons were normal. Our study identifies biophysical impairments underlying a deleterious Nav1.1 mutation and supports the hypothesis that Dravet Syndrome arises from defective inhibitory neurons.<\/jats:p>","DOI":"10.7554\/elife.13073","type":"journal-article","created":{"date-parts":[[2016,7,25]],"date-time":"2016-07-25T19:59:29Z","timestamp":1469476769000},"source":"Crossref","is-referenced-by-count":128,"title":["A deleterious Nav1.1 mutation selectively impairs telencephalic inhibitory neurons derived from Dravet Syndrome patients"],"prefix":"10.7554","volume":"5","author":[{"given":"Yishan","family":"Sun","sequence":"first","affiliation":[{"name":"Novartis Institutes for BioMedical Research, Cambridge, United States"},{"name":"Department of Neurobiology, Stanford University School of Medicine, Stanford, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sergiu P","family":"Pa\u015fca","sequence":"additional","affiliation":[{"name":"Department of Neurobiology, Stanford 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