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Depletion of intracellular calcium stores activates a calcium current in mast cells.

Authors :
Hoth M
Penner R
Source :
Nature [Nature] 1992 Jan 23; Vol. 355 (6358), pp. 353-6.
Publication Year :
1992

Abstract

In many cell types, receptor-mediated Ca2+ release from internal stores is followed by Ca2+ influx across the plasma membrane. The sustained entry of Ca2+ is thought to result partly from the depletion of intracellular Ca2+ pools. Most investigations have characterized Ca2+ influx indirectly by measuring Ca(2+)-activated currents or using Fura-2 quenching by Mn2+, which in some cells enters the cells by the same influx pathway. But only a few studies have investigated this Ca2+ entry pathway more directly. We have combined patch-clamp and Fura-2 measurements to monitor membrane currents in mast cells under conditions where intracellular Ca2+ stores were emptied by either inositol 1,4,5-trisphosphate, ionomycin, or excess of the Ca2+ chelator EGTA. The depletion of Ca2+ pools by these independent mechanisms commonly induced activation of a sustained calcium inward current that was highly selective for Ca2+ ions over Ba2+, Sr2+ and Mn2+. This Ca2+ current, which we term ICRAC (calcium release-activated calcium), is not voltage-activated and shows a characteristic inward rectification. It may be the mechanism by which electrically nonexcitable cells maintain raised intracellular Ca2+ concentrations and replenish their empty Ca2+ stores after receptor stimulation.

Details

Language :
English
ISSN :
0028-0836
Volume :
355
Issue :
6358
Database :
MEDLINE
Journal :
Nature
Publication Type :
Academic Journal
Accession number :
1309940
Full Text :
https://doi.org/10.1038/355353a0