HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Adam-Vizi, V Articles by Ligeti, E Search for Related Content PubMed PubMed Citation Articles by Adam-Vizi, V Articles by Ligeti, E

The uptake of 45Ca2+ was measured in brain synaptosomes under conditions designed to depolarize the membranes. Membrane potential was estimated from the distribution of 86Rb+ between the intra- and extracellular compartments. K+ depolarization (8-60 mM) only increased "a2+ uptake beyond a threshold depolarization of about 10 mV, whereas veratridine (5-40 microM) induced an increased Ca2+ uptake at a concentration which depolarized the membrane less than this threshold. Ouabain did not enhance Ca2+ uptake, but the depolarization it produced did not reach threshold. Ca2+ influx already stimulated by K+ depolarization can be further enhanced by veratridine without any parallel change in membrane potential. Only the pathway mediating Ca2+ uptake during K+ depolarization can be inactivated: Ca2+ uptake evoked by K+ depolarization is decreased in synaptosomes pre-depolarized in the presence of a high concentration of K+. In contrast, pre-depolarization does not change Ca2+ uptake evoked by veratridine. Ca2+ channel blockers, such as verapamil and diltiazem but not nifedipine, in concentrations of 10-100 microM, decrease the stimulation of Ca2+ uptake by high K+ concentration without influencing depolarization, whereas the effect of veratridine on Ca2+ uptake is only inhibited when its effect on Na+ channels is also prevented. It is concluded that Ca2+ uptake during K+ depolarization proceeds through voltage-dependent Ca2+ channels similar to those of squid axon, whereas veratridine activates an additional Ca2+ entry, possibly via influx through open Na+ channels. Different quantitative relationships are found between acetylcholine release of synaptosomes and the amount of Ca2+ taken up by different mechanisms: the same amount of Ca2+ uptake is accompanied by a greater increase of acetylcholine release if the uptake is induced by K+ depolarization rather than veratridine.

This article has been cited by other articles:

				C. Chinopoulos, L. Tretter, A. Rozsa, and V. Adam-Vizi Exacerbated Responses to Oxidative Stress by an Na+ Load in Isolated Nerve Terminals: the Role of ATP Depletion and Rise of [Ca2+]i J. Neurosci., March 15, 2000; 20(6): 2094 - 2103. [Abstract] [Full Text] [PDF]

				W. Meder, K. Fink, J. Zentner, and M. Göthert Calcium Channels Involved in K+- and Veratridine-Induced Increase of Cytosolic Calcium Concentration in Human Cerebral Cortical Synaptosomes J. Pharmacol. Exp. Ther., September 1, 1999; 290(3): 1126 - 1131. [Abstract] [Full Text]

				L. Tretter, C. Chinopoulos, and V. Adam-Vizi Plasma Membrane Depolarization and Disturbed Na+ Homeostasis Induced by the Protonophore Carbonyl Cyanide-p-trifluoromethoxyphenyl-hydrazon in Isolated Nerve Terminals Mol. Pharmacol., April 1, 1998; 53(4): 734 - 741. [Abstract] [Full Text]