J Pharmacol Exp Ther 1983 Jul 01;2261:269-75.

Effect of grayanotoxin on the frog neuromuscular junction.

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The effect of alpha-dihydrograyanotoxin II (alpha-H2-GTX II) on the neuromuscular junction of the frog was examined by the intracellular microelectrode technique. alpha-H2-GTX II (6 microM), with a latency of about 20 min, caused a depolarization of both the end-plate and non-end-plate region of the muscle fiber. Concomitantly, alpha-H2-GTX II caused a marked increase in the frequency of m.e.p.p.s, which persisted for 1 hr; thereafter m.e.p.p.s were gradually abolished. In end-plates which had become quiescent after treatment with alpha-H2-GTX II, synaptic vesicles could no longer be recognized histologically, suggesting that alpha-H2-GTX II depleted the store of vesicles. alpha-H2-GTX II did not affect the iontophoretically evoked acetylcholine potential, suggesting that the toxin did not greatly alter the sensitivity of the end-plate membrane to acetylcholine. Removal of Ca++ from the external medium prevented alpha-H2-GTX II from discharging synaptic vesicles. Application of tetrodotoxin or removal of Na+ ions before exposure to alpha-H2-GTX II prevented both the toxin-induced depolarization and increase in m.e.p.p. frequency. It is concluded that the action of GTX on the neuromuscular junction is probably due to an increase in membrane permeability to Na+, resulting in depolarization of both the presynaptic and postsynaptic membranes.

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