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Store‐Operated Ca 2+ Influx and Voltage‐Gated Ca 2+ Channels Coupled to Exocytosis in Pheochromocytoma (PC12) Cells
Author(s) -
Taylor S. C.,
Peers C.
Publication year - 1999
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1999.0730874.x
Subject(s) - exocytosis , extracellular , caffeine , secretion , voltage dependent calcium channel , chemistry , biophysics , depolarization , chromaffin cell , catecholamine , membrane potential , calcium , medicine , endocrinology , biology , biochemistry , adrenal medulla , organic chemistry
: Microamperometry was used to monitor quantal catecholamine release from individual PC12 cells in response to raised extracellular K + and caffeine. K + ‐evoked exocytosis was entirely dependent on Ca 2+ influx through voltage‐gated Ca 2+ channels, and of the subtypes of such channels present in these cells, influx through N‐type was primarily responsible for triggering exocytosis. L‐type channels played a minor role in mediating K + ‐evoked secretion, whereas P/Q‐type channels did not appear to be involved in secretion at all. Caffeine also evoked catecholamine release from PC12 cells, but only in the presence of extracellular Ca 2+ . Application of caffeine in Ca 2+ ‐free solutions evoked large, transient rises of [Ca 2+ ] i , but did not trigger exocytosis. When Ca 2+ was restored to the extracellular solution (in the absence of caffeine), store‐operated Ca 2+ influx was observed, which evoked exocytosis. The amount of secretion evoked by this influx pathway was far greater than release triggered by influx through L‐type Ca 2+ channels, but less than that caused by Ca 2+ influx through N‐type channels. Our results indicate that exocytosis may be regulated even in excitable cells by Ca 2+ influx through pathways other than voltage‐gated Ca 2+ channels.