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pubmed-article:8220175pubmed:abstractTextA combination of the stopped-flow technology with dual channel spectrofluorometry of Ca(2+)-indicators was utilized for the measurement of rapid Ca(2+)-signals in rat cerebral cortical synaptosomes evoked by K(+)-depolarization. There was no observable contribution of Ca(2+)-ions from intracellular stores to the rise in [Ca2+]i. The kinetics of the fast increase in intracellular Ca2+ concentration was analysed in relation to the depolarization strength. The maximal increase in [Ca2+]i and the time course of Ca(2+)-channel inactivation were determined for depolarizations obtained by different extracellular K(+)-concentrations ([K+]o). An apparent threshold was observed at about 18 mM [K+]o; a maximal Ca(2+)-signal amplitude was estimated at about 40 mM [K+]o. Pharmacological properties of the involved Ca(2+)-channels were determined using selective Ca(2+)-channel blockers (Dihydropyridines, omega-Conotoxin, omega-Agatoxins); the results suggest that a P-type voltage-dependent Ca(2+)-channel is the relevant channel type, generating the evoked Ca(2+)-signals in rat cerebral cortical synaptosomes.lld:pubmed
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pubmed-article:8220175pubmed:articleTitleAnalysis of rapid calcium signals in synaptosomes.lld:pubmed
pubmed-article:8220175pubmed:affiliationUniversity Stuttgart-Hohenheim, Institute of Zoophysiology, Germany.lld:pubmed
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pubmed-article:8220175pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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