Back to Search
Start Over
Depletion of intracellular calcium stores activates a calcium current in mast cells.
- 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.
- Subjects :
- Animals
Calcium Channel Blockers pharmacology
Calcium Channels drug effects
Cations, Divalent
Cell Membrane Permeability drug effects
Cells, Cultured
Egtazic Acid analogs & derivatives
Egtazic Acid pharmacology
Ionomycin pharmacology
Mast Cells drug effects
Membrane Potentials drug effects
Rats
Terpenes pharmacology
Thapsigargin
Calcium metabolism
Calcium Channels physiology
Inositol 1,4,5-Trisphosphate pharmacology
Mast Cells physiology
Subjects
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