Tityustoxin-mediated Na+ influx is more efficient than KCl depolarisation in promoting Ca(2+)-dependent glutamate release from synaptosomes.

The scorpion venom toxin, tityustoxin (TsTX), causes rapid, dose-dependent increases in intracellular free Ca2+ ([Ca2+]i) and glutamate release in rat cerebrocortical synaptosomes. These effects are completely abolished by the Na+ channel blocker tetrodotoxin (TTX). The increase in [Ca2+]i is completely dependent on extracellular Ca2+ but the increased glutamate release has both Ca(2+)-dependent and -independent components. Comparison of the effects of TsTX with those of depolarising concentrations of KCl reveals that TsTX is more effective, both in raising [Ca2+]i and promoting Ca(2+)-dependent and -independent glutamate release. These data suggest that the Ca(2+)-dependent glutamate release caused by TsTX is only partly due to Ca2+ entry through voltage-sensitive Ca2+ channels.