Atp depletion inhibits capacitative ca2+ entry in rat thymic
lymphocytes.
Marriott, Ian, and Michael J. Mason.
Department of Physiology, Tulane University School of Medicine, New
Orleans, LA 70112.
APStracts 2:0172C, 1995.
The present study investigates the requirement for cellular ATP in the
increase in plasma membrane Ca2+ permeability activated by the
release of Ca2+ from intracellular stores in rat thymic lymphocytes
(Capacitative Ca2+ Entry). The permeability state of this pathway
following activation with thapsigargin was probed in control and ATP
-depleted cells using fluorometric measurements of [Ca2+]i, Mn2+
entry, and membrane potential, and unidirectional measurements of
Ca2+ uptake using 45Ca2+. The capacitative Ca2+ entry pathway was
markedly inhibited in cells depleted of ATP by incubation in glucose
-free solution containing oligomycin, antimycin A and 2-deoxy-D
-glucose. These data cannot be explained on the basis of a loss of the
transmembrane electrochemical gradient for Ca2+, alterations in
intracellular pH or cellular Na+ content, a direct effect of the
inhibitors of ATP production on the capacitative Ca2+ entry pathway,
or the ability of thapsigargin to release Ca2+ from intracellular
stores. Rather, these data are consistent with a requirement for ATP
or a high energy phosphate donor in the activation and/or maintained
activation of capacitative Ca2+ entry.
Received 5 January 1995; accepted in final form 11 April 1995.
APS Manuscript Number C11-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.