Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode.

Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode. Research Abstract Details 

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Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode. Abstract Text:

Murali Prakriya,Richard S Lewis,

CRAC (calcium release-activated Ca(2+)) channels attain an extremely high selectivity for Ca(2+) from the blockade of monovalent cation permeation by Ca(2+) within the pore. In this study we have exploited the blockade by Ca(2+) to examine the size of the CRAC channel pore, its unitary conductance for monovalent cations, and channel gating properties. The permeation of a series of methylammonium compounds under divalent cation-free conditions indicates a minimum pore diameter of 3.9 A. Extracellular Ca(2+) blocks monovalent flux in a manner consistent with a single intrapore site having an effective K(i) of 20 microM at -110 mV. Block increases with hyperpolarization, but declines below -100 mV, most likely due to permeation of Ca(2+). Analysis of monovalent current noise induced by increasing levels of block by extracellular Ca(2+) indicates an open probability (P(o)) of approximately 0.8. By extrapolating the variance/mean current ratio to the condition of full blockade (P(o) = 0), we estimate a unitary conductance of approximately 0.7 pS for Na(+), or three to fourfold higher than previous estimates. Removal of extracellular Ca(2+) causes the monovalent current to decline over tens of seconds, a process termed depotentiation. The declining current appears to result from a reduction in the number of active channels without a change in their high open probability. Similarly, low concentrations of 2-APB that enhance I(CRAC) increase the number of active channels while open probability remains constant. We conclude that the slow regulation of whole-cell CRAC current by store depletion, extracellular Ca(2+), and 2-APB involves the stepwise recruitment of silent channels to a high open-probability gating mode.

Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode. Publishing Authors By Initials

M Prakriya,RS Lewis,

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Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode. Journal Published:

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

Journal: The Journal of general physiology

VOLUME: 128

Page Numbers: 373-86

Journal Abbreviation:

ISSN: 0022-1295

DAY: 3

MONTH: Sep

YEAR: 2006

Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode. Information

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LANGUAGE: eng

NlmUniqueID: 2985110

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Grant and Affiliation Information for Regulation of CRAC channel activity by recruitment of silent channels to a high open-probability gating mode.

AFFILIATION: Department of Molecular and Cellular Physiology, Stanford University School of Medicine, Stanford, CA 94305, USA. m-prakriya@northwestern.edu

Country: United States

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MEDLINETA: J Gen Physiol

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