ANALYSIS OF RAPID CALCIUM SIGNALS IN SYNAPTOSOMES

A combination of the stopped-flow technology with dual channel spectro fluorometry of Ca2+-indicators was utilized for the measurement of rap id Ca2+-signals in rat cerebral cortical synaptosomes evoked by K+-dep olarization. There was no observable contribution of Ca2+-ions from in tracellular stores to the rise in [Ca2+]i. The kinetics of the fast in crease in intracellular Ca2+ concentration was analysed in relation to the depolarization strength. The maximal increase in [Ca2+]i and the time course of Ca2+-channel inactivation were determined for depolariz ations obtained by different extracellular K+-concentrations ([K+]o). An apparent threshold was observed at about 18 mM [K+]o; a maximal Ca2 +-signal amplitude was estimated at about 40 mM [K+]o. Pharmacological properties of the involved Ca2+-channels were determined using select ive Ca2+-channel blockers (Dihydropyridines, omega-Conotoxin, omega-Ag atoxins); the results suggest that a P-type voltage-dependent Ca2+-cha nnel is the relevant channel type, generating the evoked Ca2+-signals in rat cerebral cortical synaptosomes.