[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.