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J. Biol. Chem., Vol. 268, Issue 30, 22262-22264, Oct, 1993
CC Petersen, OH Petersen and MJ Berridge
Many cell types show repetitive short lasting cytosolic calcium spikes with
long interspike periods when stimulated with submaximal concentrations of
agonists linked to the phosphoinositide signaling pathway. In pancreatic
acinar cells these spikes have been shown to be evoked by constant levels
of inositol trisphosphate through a mechanism of calcium-induced calcium
release and do not depend acutely on the presence of external calcium.
However, the processes involved in the interspike period have remained
unclear. Here we report that the endoplasmic reticulum Ca(2+)-ATPase play a
significant role, not only in resequestering calcium after a spike, but
also in regulating the long interspike period. Decreasing the activity of
the endoplasmic reticulum calcium pumps leads to shorter interspike
intervals and thus higher spiking frequencies, while the duration of each
spike increases. The endoplasmic reticulum Ca(2+)-ATPases are able to
entirely suppress a response that can subsequently be evoked by partial
inhibition of the pumps. This suggests that during the interspike period
there is a considerable amount of calcium released from intracellular
stores, which is rapidly buffered by the endoplasmic reticulum calcium
pumps and the cytosolic calcium-binding proteins. A calcium spike will be
initiated by calcium-induced calcium release only when the buffering is
saturated.
The role of endoplasmic reticulum calcium pumps during cytosolic calcium spiking in pancreatic acinar cells
Department of Zoology, University of Cambridge, United Kingdom.
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