[Mechanisms of calcium transport in brain synaptosomes as affected by depolarization].
Data of the inhibitory analysis suggest that the increase in the content of calcium in veratrine-, ouabain- and 80 mM K+-depolarized synaptosomes is due to Ca2+ influx through the potential-dependent calcium channels. The decrease of the intracellular concentration of Ca2+ in depolarized nerve endings is mainly caused by the calmodulin-dependent Ca,Mg-ATPase of synaptolemma and mitochondria. The regularities of ATP-dependent Ca2+ transport in synaptosomal plasma membranes were studied on the microsomes whose properties were found identical to those of native synaptolemma. A comparison of the kinetic parameters of Ca-transport systems in brain microsomes and mitochondria and the data on extensive inhibition of 45Ca uptake by rotenone and oligomycin suggest that mitochondria play a key role in the control of intraterminal concentration of Ca2+ during nerve impulse conduction.
D000818:Animals; D001921:Brain / Q000201:enzymology*; D017301:Ca(2+) Mg(2+)-ATPase; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000378:metabolism*; D002147:Calmodulin / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D008928:Mitochondria / Q000201:enzymology; D008954:Models, Biological; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D051381:Rats; D013574:Synaptosomes / Q000187:drug effects / Q000201:enzymology* / Q000502:physiology; D014701:Veratridine / Q000494:pharmacology
D002147:Calmodulin; D010042:Ouabain; D014701:Veratridine; D017301:Ca(2+) Mg(2+)-ATPase; D000252:Calcium-Transporting ATPases; D011188:Potassium; D002118:Calcium
Mekhanizmy transporta kal'tsiia v sinaptosomakh golovnogo mozga v usloviiakh depoliarizatsii.