Depleted internal store-activated Ca2+ entry can trigger neurotransmitter release in bovine chromaffin cells.
A potential role of the intracellular Ca2+ stores in modulating catecholamine release has been investigated in bovine chromaffin cells maintained in tissue culture. Pharmacological depletion of the stores with a combination of caffeine, histamine and thapsigargin in Ca2+-free media resulted in a significantly greater release of catecholamines on re-exposure to Ca2+-containing media compared with that from non-store depleted cells. The increase in catecholamine release was prevented by intracellular BAPTA indicating that the increase was caused by a rise in Ca2+. Measurement of intracellular free Ca2+ concentration with the fluorescent indicator, fura-2, over the same time-course as the catecholamine release experiments showed that upon restoration of external Ca2+ there was an immediate, substantial and maintained increase in cytosolic Ca2+. It is most probable that the increase in catecholamine release was a consequence of an increase in Ca2+ influx triggered by prior depletion of the internal Ca2+ stores. However, the data suggest that capacitative Ca2+ entry is poorly linked to catecholamine release; although Ca2+ entry on restoration of external Ca2+ was immediate and substantial, the increase in catecholamine release, although quantitatively significant, was slowly realised.
Powis
D A
DA
The Neuroscience Group, Faculty of Medicine and Health Sciences, University of Newcastle, New South Wales, Australia.
Clark
C L
CL
O'Brien
K J
KJ
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002395:Catecholamines / Q000378:metabolism*; D002417:Cattle; D002478:Cells, Cultured / Q000378:metabolism; D002838:Chromaffin System / Q000166:cytology*; D004791:Enzyme Inhibitors; D016257:Fura-2; D018377:Neurotransmitter Agents / Q000378:metabolism; D019284:Thapsigargin
D002395:Catecholamines; D004791:Enzyme Inhibitors; D018377:Neurotransmitter Agents; D019284:Thapsigargin; D002118:Calcium; D016257:Fura-2