HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (25) Citing Articles via Google Scholar Google Scholar Articles by Ulbricht, W. Search for Related Content PubMed PubMed Citation Articles by Ulbricht, W.

Sodium Channel Inactivation: Molecular Determinants and Modulation

Physiologisches Institut, University of Kiel, Kiel, Germany

Voltage-gated sodium channels open (activate) when the membrane is depolarized and close on repolarization (deactivate) but also on continuing depolarization by a process termed inactivation, which leaves the channel refractory, i.e., unable to open again for a period of time. In the "classical" fast inactivation, this time is of the millisecond range, but it can last much longer (up to seconds) in a different slow type of inactivation. These two types of inactivation have different mechanisms located in different parts of the channel molecule: the fast inactivation at the cytoplasmic pore opening which can be closed by a hinged lid, the slow inactivation in other parts involving conformational changes of the pore. Fast inactivation is highly vulnerable and affected by many chemical agents, toxins, and proteolytic enzymes but also by the presence of -subunits of the channel molecule. Systematic studies of these modulating factors and of the effects of point mutations (experimental and in hereditary diseases) in the channel molecule have yielded a fairly consistent picture of the molecular background of fast inactivation, which for the slow inactivation is still lacking.

This article has been cited by other articles:

				A. H. Gittis and S. du Lac Similar Properties of Transient, Persistent, and Resurgent Na Currents in GABAergic and Non-GABAergic Vestibular Nucleus Neurons J Neurophysiol, May 1, 2008; 99(5): 2060 - 2065. [Abstract] [Full Text] [PDF]

				L. Bocchi and M. Vassalle Characterization of the slowly inactivating sodium current INa2 in canine cardiac single Purkinje cells Exp Physiol, March 1, 2008; 93(3): 347 - 361. [Abstract] [Full Text] [PDF]

				D. B. Tikhonov and B. S. Zhorov Sodium Channels: Ionic Model of Slow Inactivation and State-Dependent Drug Binding Biophys. J., September 1, 2007; 93(5): 1557 - 1570. [Abstract] [Full Text] [PDF]

				A. M. Rush, T. R. Cummins, and S. G. Waxman Multiple sodium channels and their roles in electrogenesis within dorsal root ganglion neurons J. Physiol., February 15, 2007; 579(1): 1 - 14. [Abstract] [Full Text] [PDF]

				E. E. Benarroch Sodium channels and pain Neurology, January 16, 2007; 68(3): 233 - 236. [Full Text] [PDF]

				C. Maertens, E. Cuypers, M. Amininasab, A. Jalali, H. Vatanpour, and J. Tytgat Potent Modulation of the Voltage-Gated Sodium Channel Nav1.7 by OD1, a Toxin from the Scorpion Odonthobuthus doriae Mol. Pharmacol., July 1, 2006; 70(1): 405 - 414. [Abstract] [Full Text] [PDF]

				S.-Y. Wang, J. Mitchell, D. B. Tikhonov, B. S. Zhorov, and G. K. Wang How Batrachotoxin Modifies the Sodium Channel Permeation Pathway: Computer Modeling and Site-Directed Mutagenesis Mol. Pharmacol., March 1, 2006; 69(3): 788 - 795. [Abstract] [Full Text] [PDF]