Autor: |
Taylor, Shafeena C., Peers, Chris |
Předmět: |
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Zdroj: |
Journal of Neurochemistry; Oct2000, Vol. 75 Issue 4, p1583-1589, 7p |
Abstrakt: |
Abstract: Amperometry and microfluorimetry were employed to investigate the Ca2+-dependence of catecholamine release induced from PC12 cells by cholinergic agonists. Nicotine-evoked exocytosis was entirely dependent on extracellular Ca2+ but was only partly blocked by Cd2+, a nonselective blocker of voltagegated Ca2+ channels. Secretion and rises of [Ca2+]i observed in response to nicotine could be almost completely blocked by methyllycaconitine and α-bungarotoxin, indicating that such release was mediated by receptors composed of α7 nicotinic acetylcholine receptor subunits. Secretion and [Ca2+]i rises could also be fully blocked by co-application of Cd2+ and Zn2+. Release evoked by muscarine was also fully dependent on extracellular Ca2+. Muscarinic receptor activation stimulated release of Ca2+ from a caffeine-sensitive intracellular store, and release from this store induced capacitative Ca2+ entry that could be blocked by La3+ and Zn2+. This Ca2+ entry pathway mediated all secretion evoked by muscarine. Thus, activation of acetylcholine receptors stimulated rises of [Ca2+]i and exocytosis via Ca2+ influx through voltage-gated Ca2+ channels, α7 subunit-containing nicotinic acetylcholine receptors, and channels underlying capacitative Ca2+ entry. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
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