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- W2001967573 abstract "Classic calcium hypothesis states that depolarization-induced increase in intracellular Ca2+ concentration ([Ca2+]i) triggers vesicle exocytosis by increasing vesicle release probability in neurons and neuroendocrine cells. The extracellular Ca2+, in this calcium hypothesis, serves as a reservoir of Ca2+ source. Recently we find that extracellular Ca2+ per se inhibits the [Ca2+]i dependent vesicle exocytosis, but it remains unclear whether quantal size is regulated by extracellular, or intracellular Ca2+ or both [1]. In this work we showed that, in physiological condition, extracellular Ca2+ per se specifically inhibited the quantal size of single vesicle release in rat adrenal slice chromaffin cells. The extracellular Ca2+ in physiological concentration (2.5 mM) directly regulated fusion pore kinetics of spontaneous quantal release of catecholamine. In addition, removal of extracellular Ca2+ directly triggered vesicle exocytosis without eliciting intracellular Ca2+. We propose that intracellular Ca2+ and extracellular Ca2+ per se cooperately regulate single vesicle exocytosis. The vesicle release probability was jointly modulated by both intracellular and extracellular Ca2+, while the vesicle quantal size was mainly determined by extracellular Ca2+ in chromaffin cells physiologically." @default.
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- W2001967573 date "2014-09-01" @default.
- W2001967573 modified "2023-10-16" @default.
- W2001967573 title "Extracellular Ca2+ per se inhibits quantal size of catecholamine release in adrenal slice chromaffin cells" @default.
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- W2001967573 doi "https://doi.org/10.1016/j.ceca.2014.07.006" @default.
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