BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism.

BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism. Research Abstract Details 

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BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism. Abstract Text:

Xu-Hui Zeng,G Richard Benzinger,Xiao-Ming Xia,Christopher J Lingle,

Large-conductance, Ca2+- and voltage-activated K+ (BK) channels are broadly expressed proteins that respond to both cellular depolarization and elevations in cytosolic Ca2+. The characteristic functional properties of BK channels among different cells are determined, in part, by tissue-specific expression of auxiliary beta subunits. One important functional property conferred on BK channels by beta subunits is inactivation. Yet, the physiological role of BK channel inactivation remains poorly understood. Here we report that as a consequence of a specific mechanism of inactivation, BK channels containing the beta3a auxiliary subunit exhibit an anomalous slowing of channel closing. This produces a net repolarizing current flux that markedly exceeds that expected if all open channels had simply closed. Because of the time dependence of inactivation, this behavior results in a Ca2+-independent but time-dependent increase in a slow tail current, providing an unexpected mechanism by which use-dependent changes in slow afterhyperpolarizations might regulate electrical firing. The physiological significance of inactivation in BK channels mediated by different beta subunits may therefore arise not from inactivation itself, but from the differences in the amplitude and duration of repolarizing currents arising from the beta-subunit-specific energetics of recovery from inactivation.

BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism. Publishing Authors By Initials

XH Zeng,GR Benzinger,XM Xia,CJ Lingle,

For similar proteins: protein subunits research abstracts see: proteins: protein subunits research

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BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of neuroscience : the official journal

VOLUME: 27

Page Numbers: 4707-15

Journal Abbreviation:

ISSN: 1529-2401

DAY: 25

MONTH: Apr

YEAR: 2007

BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism. Information

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LANGUAGE: eng

NlmUniqueID: 8102140

BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism. Keywords Mesh Terms:

KEYWORDS: Protein Subunits

MESH TERMS: physiology

Chemical & Substance for Abstract: BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism. Information

Substance Name: Calcium

Registry Number: 7440-70-2

Grant and Affiliation Information for BK channels with beta3a subunits generate use-dependent slow afterhyperpolarizing currents by an inactivation-coupled mechanism.

AFFILIATION: Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.

Country: United States

AGENCY: United States NIGMS

GRANT: GM068580

ACRONYM: GM

MEDLINETA: J Neurosci

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