NDLI: Reduced sodium channel density, altered voltage dependence of inactivation, and increased susceptibility to seizures in mice lacking sodium channel beta 2-subunits.

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Reduced sodium channel density, altered voltage dependence of inactivation, and increased susceptibility to seizures in mice lacking sodium channel beta 2-subunits.

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Reduced sodium channel density, altered voltage dependence of inactivation, and increased susceptibility to seizures in mice lacking sodium channel beta 2-subunits.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Avery, Christy Kazarinova-noyes, Katie Chen, Yuan Macdonald, Robert L. Bharucha, Vandana Catterall, William A. Malhotra, Jyoti Dhar Ransom, Bruce R. Brown, Angus Scheuer, Todd Westenbroek, Ruth E. Shrager, Peter Isom, Lori L. Saunders, Thomas L. Chen, Chunling Jones, Dorothy Kazen-gillespie, Kristin A. Gillespie, Patrick J.
Description	Author Affiliation: Chen C ( Departments of Pharmacology and Neurology, and Transgenic Animal Model Core Laboratory, University of Michigan, Ann Arbor, MI 48109, USA.);
Abstract	Sodium channel beta-subunits modulate channel gating, assembly, and cell surface expression in heterologous cell systems. We generated beta2(-/-) mice to investigate the role of beta2 in control of sodium channel density, localization, and function in neurons in vivo. Measurements of [(3)H]saxitoxin (STX) binding showed a significant reduction in the level of plasma membrane sodium channels in beta2(-/-) neurons. The loss of beta2 resulted in negative shifts in the voltage dependence of inactivation as well as significant decreases in sodium current density in acutely dissociated hippocampal neurons. The integral of the compound action potential in optic nerve was significantly reduced, and the threshold for action potential generation was increased, indicating a reduction in the level of functional plasma membrane sodium channels. In contrast, the conduction velocity, the number and size of axons in the optic nerve, and the specific localization of Na(v)1.6 channels in the nodes of Ranvier were unchanged. beta2(-/-) mice displayed increased susceptibility to seizures, as indicated by reduced latency and threshold for pilocarpine-induced seizures, but seemed normal in other neurological tests. Our observations show that beta2-subunits play an important role in the regulation of sodium channel density and function in neurons in vivo and are required for normal action potential generation and control of excitability.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	26
Volume Number	99
Language	English
Publisher	National Academy of Sciences
Publisher Date	2002-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Seizures Etiology Sodium Channels Physiology Action Potentials Animals Disease Susceptibility Mice Mice, Knockout Nerve Fibers Neural Conduction Pilocarpine Pharmacology Protein Subunits Sodium Metabolism Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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