Abstract

d-Tubocurarine and the α-neurotoxins from snake venom are antagonists at the nicotinic acetylcholine receptor. It is well established that d-tubocurarine causes fade in neuromuscular transmission during repetitive nerve stimulation but paradoxically there are many reports which indicate that the α-neurotoxins do not cause such fade. We found that high concentrations of erabutoxin b (100–150 nM) from the venom of Laticauda semifasciata did not cause much fade in the rat diaphragm preparation. However, low concentrations of toxin (5 nM) caused severe fade which was similar to the effects of d-tubocurarine. The data suggest that fade may be caused by toxin binding to a high-affinity site on the postsynaptic acetylcholine receptor.

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