Inhibition of K(+)-evoked [3H]D-aspartate release and neuronal calcium influx by verapamil, diltiazem and dextromethorphan: evidence for non-L/non-N voltage-sensitive calcium channels.

摘要: The effects of inhibitors voltage-sensitive calcium channels (VSCC) on K(+)-evoked [3H]D-aspartate release from rat hippocampal slices and the increase in intracellular neocortical neurons primary culture were examined. K+ caused a concentration-dependent that was approximately 85% dependent presence extracellular calcium. Neither marine snail toxin, omega-conotoxin GVIA, nor dihydropyridine VSCC antagonist, nitrendipine, had any effect [3H]D-aspartate. omega-Conotoxin GVIA nitrendipine relatively small (20-30%) inhibition culture. This suggests is not L- or N-type VSCC, whereas neuronal influx only partially VSCC. Verapamil, dextromethorphan diltiazem with IC50 values 30, 100 120 microM, respectively. inhibited essentially same rank order potency, but slightly greater potencies (IC50 for verapamil, 20, 50 respectively). At 300 neither evoked by ionophore ionomycin, suggesting these compounds are acting intracellularly to inhibit ability free cytosolic evoke release.(ABSTRACT TRUNCATED AT 250 WORDS)