KCNK2: Reversible conversion of a hippocampal potassium leak into a voltage-dependent channel

Detlef Bockenhauer; Noam Zilberberg; S. A.N. Goldstein

doi:10.1038/87434

KCNK2: Reversible conversion of a hippocampal potassium leak into a voltage-dependent channel

Detlef Bockenhauer, Noam Zilberberg, S. A.N. Goldstein

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147 Scopus citations

Abstract

Potassium leak channels are essential to neurophysiological function. Leaks suppress excitability through maintenance of resting membrane potential below the threshold for action potential firing. Conversely, voltage-dependent potassium channels permit excitation because they do not interfere with rise to threshold, and they actively promote recovery and rapid re-firing. Previously attributed to distinct transport pathways, we demonstrate here that phosphorylation of single, native hippocampal and cloned KCNK2 potassium channels produces reversible interconversion between leak and voltage-dependent phenotypes. The findings reveal a pathway for dynamic regulation of excitability.

Original language	English
Pages (from-to)	486-491
Number of pages	6
Journal	Nature Neuroscience
Volume	4
Issue number	5
DOIs	https://doi.org/10.1038/87434
State	Published - 1 Jan 2001
Externally published	Yes

ASJC Scopus subject areas

General Neuroscience

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title = "KCNK2: Reversible conversion of a hippocampal potassium leak into a voltage-dependent channel",

abstract = "Potassium leak channels are essential to neurophysiological function. Leaks suppress excitability through maintenance of resting membrane potential below the threshold for action potential firing. Conversely, voltage-dependent potassium channels permit excitation because they do not interfere with rise to threshold, and they actively promote recovery and rapid re-firing. Previously attributed to distinct transport pathways, we demonstrate here that phosphorylation of single, native hippocampal and cloned KCNK2 potassium channels produces reversible interconversion between leak and voltage-dependent phenotypes. The findings reveal a pathway for dynamic regulation of excitability.",

author = "Detlef Bockenhauer and Noam Zilberberg and Goldstein, {S. A.N.}",

note = "Funding Information: This work was supported by grants to S.A.N.G. from the National Institutes of Health. D.B. is supported by the Child Health Research Center (Yale University)",

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AU - Goldstein, S. A.N.

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N2 - Potassium leak channels are essential to neurophysiological function. Leaks suppress excitability through maintenance of resting membrane potential below the threshold for action potential firing. Conversely, voltage-dependent potassium channels permit excitation because they do not interfere with rise to threshold, and they actively promote recovery and rapid re-firing. Previously attributed to distinct transport pathways, we demonstrate here that phosphorylation of single, native hippocampal and cloned KCNK2 potassium channels produces reversible interconversion between leak and voltage-dependent phenotypes. The findings reveal a pathway for dynamic regulation of excitability.

AB - Potassium leak channels are essential to neurophysiological function. Leaks suppress excitability through maintenance of resting membrane potential below the threshold for action potential firing. Conversely, voltage-dependent potassium channels permit excitation because they do not interfere with rise to threshold, and they actively promote recovery and rapid re-firing. Previously attributed to distinct transport pathways, we demonstrate here that phosphorylation of single, native hippocampal and cloned KCNK2 potassium channels produces reversible interconversion between leak and voltage-dependent phenotypes. The findings reveal a pathway for dynamic regulation of excitability.

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KCNK2: Reversible conversion of a hippocampal potassium leak into a voltage-dependent channel

Abstract

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