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J. Biol. Chem., Vol. 269, Issue 20, 14359-14362, May, 1994
JF Worley 3rd, MS McIntyre, B Spencer, RJ Mertz, MW Roe and ID Dukes
Glucose stimulation of islet beta-cell insulin secretion is initiated by
membrane depolarization and an elevation in intracellular free calcium
concentration ([Ca2+]i) from a combination of influx through
depolarization-activated Ca2+ channels and intracellular Ca2+ store
release. Prevention of Ca2+ store refilling with thapsigargin produced a
sustained depolarization, leading to enhanced Ca2+ influx and an elevation
in [Ca2+]i in 12 mM glucose. Depletion of intracellular Ca2+ stores by
external EGTA reduced [Ca2+]i and also caused a long-lasting
depolarization. In single beta-cells, external EGTA activated an inward
current, the voltage range and kinetic properties of which differed from
those of voltage-dependent Ca2+ channels. A novel pathway thus exists in
beta-cells by which depletion of endoplasmic reticulum Ca2+ stores results
in the activation of an inward current that, by inducing depolarization,
facilitates Ca2+ influx through voltage-gated Ca2+ channels. The
physiological relevance of this pathway in the control of beta-cell
function is indicated by the stimulation of insulin secretion by
thapsigargin.
Endoplasmic reticulum calcium store regulates membrane potential in mouse islet beta-cells
Department of Cell Physiology, Glaxo Research Institute, Research Triangle Park, North Carolina 27709.
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