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pubmed-article:8938256pubmed:abstractTextA 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.lld:pubmed
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pubmed-article:8938256pubmed:pagination165-8lld:pubmed
pubmed-article:8938256pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:8938256pubmed:articleTitleDepleted internal store-activated Ca2+ entry can trigger neurotransmitter release in bovine chromaffin cells.lld:pubmed
pubmed-article:8938256pubmed:affiliationThe Neuroscience Group, Faculty of Medicine and Health Sciences, University of Newcastle, New South Wales, Australia.lld:pubmed
pubmed-article:8938256pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:8938256pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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