Currents through voltage-gated sodium channels drive action potential depolarization in neurons and other excitable cells. Smaller currents through these channels are key components of currents that control neuronal firing and signal integration. Changes in sodium current have profound effects on neuronal firing. Sodium channels are controlled by neuromodulators acting through phosphorylation of the channel by serine/threonine and tyrosine protein kinases. That phosphorylation requires specific molecular interaction of kinases and phosphatases with the channel molecule to form localized signalling complexes. Such localization is required for effective neurotransmitter-mediated regulation of sodium channels by protein kinase A. Analogous molecular complexes between sodium channels, kinases and other signalling molecules are expected to be necessary for specific and localized transmitter-mediated modulation of sodium channels by other protein kinases.
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December 2006
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Conference Article|
October 25 2006
Control of neuronal excitability by phosphorylation and dephosphorylation of sodium channels
T. Scheuer;
T. Scheuer
1
1Department of Pharmacology, Mailstop 357280, University of Washington, Seattle, WA 98195-7280, U.S.A.
1To whom correspondence should be addressed (email Scheuer@u.washington.edu).
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W.A. Catterall
W.A. Catterall
1Department of Pharmacology, Mailstop 357280, University of Washington, Seattle, WA 98195-7280, U.S.A.
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Publisher: Portland Press Ltd
Received:
June 26 2006
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2006 The Biochemical Society
2006
Biochem Soc Trans (2006) 34 (6): 1299–1302.
Article history
Received:
June 26 2006
Citation
T. Scheuer, W.A. Catterall; Control of neuronal excitability by phosphorylation and dephosphorylation of sodium channels. Biochem Soc Trans 1 December 2006; 34 (6): 1299–1302. doi: https://doi.org/10.1042/BST0341299
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