Calcium-dependent Enhancement of Depletion-activated Calcium Current in Jurkat T Lymphocytes |
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Authors: | EP Christian KT Spence JA Togo PG Dargis J Patel |
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Institution: | (1) Department of Pharmacology, Zeneca Pharmaceuticals, 1800 Concord Pike, Wilmington, DE 19850, US |
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Abstract: | We have obtained evidence that the Ca2+-selective current activated by Ca2+ store depletion (Ca2+ release-activated Ca2+ current; I
crac) in Jurkat T lymphocytes is augmented in a time-dependent manner by Ca2+ itself. Whole cell patch clamp experiments employed high cytosolic Ca2+-buffering conditions to passively deplete Ca2+ stores. Rapidly switching to nominally Ca2+-free extracellular buffer instantaneously reduced I
crac measured at −100 mV to leak current level. Unexpectedly, readmission of 2 mm Ca2+ instantaneously restored only 38 ± 5% (mean ±sem; n = 9) of the full I
crac amplitude. The remainder reappeared in a monotonic time-dependent manner over 10 to 20 sec. Rapid vs. slow intracellular Ca2+ chelators did not alter this process, and inorganic I
crac blockers did not regenerate it, arguing against an intracellular site of action. The effect was specific to Ca2+: introduction of the permeant ions, Ba2+ or Sr2+, failed to invoke time-dependent I
crac reappearance. Moreover, equimolar substitution of Ba2+ for Ca2+ initially produced Ba2+ current of similar magnitude to the full Ca2+ current, but the Ba2+ current decayed monotonically to <50% of its initial amplitude in <20 sec. Conversely, return to Ca2+ produced a time-dependent increase in I
crac to its larger Ca2+ permeation level. Thus Ca2+ appears to selectively promote a reversible transition of I
crac that results in larger current flux, and at least partially explains the selectivity of this current for Ca2+ over other divalent ions.
Received: 30 August 1995/Revised: 7 November 1995 |
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Keywords: | : Ca2+ current — Depletion-activated Ca2+ current — Voltage-independent Ca2+ current — Ca2+ selectivity — Ba2+ permeation — Jurkat cell |
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