Affiliation:
1. Department of Pharmacology, University of Washington, Seattle, Washington
Abstract
Here, we utilize CRISPR/Cas9-mediated mutagenesis in dopamine neurons in mice to target the gene encoding Kvβ2, an auxiliary subunit that forms a part of Kv1 channel complexes. We find that the absence of Kvβ2 alters action potential properties by reducing surface expression of pore-forming subunits and shifting the voltage dependence of channel inactivation. This work establishes a new function for Kvβ2 subunits and Kv1 complexes in regulating dopamine neuron activity.
Funder
HHS | NIH | National Center for Advancing Translational Sciences
HHS | NIH | National Institute on Drug Abuse
HHS | NIH | NIH Office of the Director
Publisher
American Physiological Society
Subject
Physiology,General Neuroscience
Cited by
7 articles.
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