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The tritium overflow evoked by electrical stimulation of rabbit hippocampal slices labeled with [3H]noradrenaline was inhibited by omega-conotoxin GVIA, a peptide modulator of the N-type voltage-sensitive calcium channel (N-VSCC). The magnitude of this inhibition was unchanged in the presence of substances which interact with N- and/or L-VSCCs (cadmium, neomycin, (-)- and (+)-202-791), alpha 2-adrenoceptors (idazoxan, UK-14304), protein kinase C (4 beta-phorbol-12,13-dibutyrate) or potassium channels (4-aminopyridine). This finding suggests that the attenuation of calcium-dependent neurotransmitter release by omega-conotoxin GVIA is relatively insensitive to alterations of such release effected by other substances.
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