Postdoctoral Fellow

Oct 15, 2019
Nov 14, 2019
Position Type
Full Time

Postdoctoral Research Position Available

William A. Catterall

Department of Pharmacology and Neuroscience Program

University of Washington, Seattle, WA 98195-7280 USA


Sodium Channels and Autism

We found that loss-of-function mutations in the brain voltage-gated sodium channel type-1 that cause Dravet Syndrome also lead to autistic-like behaviors in mice (Han et al., 2012; Rubinstein et al., 2015). Genome sequencing of families with de novo mutations that cause autism has revealed that the gene encoding the closely related brain voltage-gated sodium channel type-2 (Nav1.2) is the most frequent target of de novo autism-causing mutations. Many of these mutations are in voltage-sensing domains of Nav1.2 channels. We plan to introduce these mutations into sodium channel cDNAs, express them at high in levels in cultured cells, and analyze their functional effects on sodium channels using whole-cell voltage clamp methods. In collaboration with Larry Zweifel (Psychiatry & Behavioral Science and Pharmacology, UW), selected mutations will be introduced into specific classes of neurons in mouse brain using CRISPR/Cas methods, and their impact on sodium channel function and cellular excitability in those neurons will be determined. Effects of the mutant Nav1.2 channels on social interaction behaviors and other autism-related phenotypes will be studied in these mice. We hope that these studies will reveal a common thread in the functional changes in Nav1.2 channels caused by these autism-inducing mutations, which will give important insight into the fundamental defects in neuronal excitability that lead to autism.


Han S, Tai C, Westenbroek RE, Yu FH, Cheah CS, Potter GB, Rubenstein JL, Scheuer T, de la Iglesia HO, Catterall WA. (2012) Autistic-like behaviour in Scn1a+/- mice and rescue by enhanced GABA-mediated neurotransmission. Nature 489:385-390.


Rubinstein M, Han S, Tai C, Westenbroek RE, Hunker A, Scheuer T, Catterall WA. (2015) Dissecting the phenotypes of Dravet syndrome by gene deletion. Brain 138:2219-2233.



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Position Requirements

Basic molecular and cellular biology, whole-cell voltage clamp physiology, and membrane biophysics.

Experience with brain slice recording and behavioral studies in rodents is valuable.

We seek enthusiastic well-trained neuroscientists who are excited about the opportunity to analyze mutations that cause autism, a widespread and devastating neuropsychiatric disease, at the molecular, cellular, and systems levels, with the hope of discovering novel therapeutic approaches.