Further characterization of phasic calcium influx in rat cerebrocortical synaptosomes: inferences regarding calcium channel type(s) in nerve endings.

Under conditions minimizing the contribution of Na+/Ca2+ exchange to calcium entry in synaptosomes, the K+ depolarization-dependent calcium influx (JCa) is a single exponential function of time. JCa activates and slowly inactivates at membrane potentials positive to -50 mV, a result indicating the involvement of moderate voltage-activating, slowly inactivating calcium channels. Calcium channels in synaptosomes are characterized by stronger sensitivity to blockage by Cd2+ than Co2+, insensitivity to dihydropyridine calcium antagonists or the agonist Bay K 8644, and weak, partial sensitivity to the peptide toxin omega-conotoxin GVIA. These characteristics suggest that voltage-sensitive calcium channels in rat cerebrocortical synaptosomes are dissimilar from the somatic T, N, or L channel types. JCa is not affected by treatment of synaptosomes with the adenylate cyclase activator forskolin, the membrane permeant dibutyryl-cyclic AMP, or the kinase C activator phorbol 12-myristate 13-acetate diester, results suggesting that calcium channels in synaptosomes are not directly modulated by protein kinase A- or C-mediated phosphorylation.