Abstract
Inhibition of the N and L type Ca 2+ channels with omega conotoxin GVIA (ω-CgTx) together with the dihydropyridine (−)-202–791 products slight reduction (≅ 25%) of K +-evoked Ca 2+ influx in mammalian synaptosomes. These results and others suggest the existence of a third high threshold voltage sensitive calcaium channel (VSCC) responsible for the majority of influx. Venom from the funnel web spider Hololena curta potently and persistently inhibited Ca 2+ influx in rat cortical synaptosomes (IC 50 1: 10,000 or 4.21 μg/venom protein/ml of synaptosomes). Also Ca 2+ influx in cerebellar synaptosomes was inhibited in a similar manner. K +-evoked tritium release from synaptosomes labeled with [ 3H]noradrenaline was inhibited by Hololena venom (≅ 60% reduction at 10 μg/venom protein). Inhibition of Ca 2+ influx by venom was unaffected by combined ω-CgTx and (−)-202–791 pretreatment (both 1 μM). Hololena venom and its active constituent should provide useful tools to investigate the role of this novel Ca 2+ channel in neuronal function.
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