Abstract

The effects of an acetylcholine analogue, carbachol (CCh), and a purified irreversible nicotinic antagonist, α-bungarotoxin (BTX), on the frequency of the miniature endplate potentials (mEPPs) at the neuromuscular junction of the frog were tested at 20 and 10¡C. CCh (5 ± 10-6 m) reduced the frequency of mEPPs to about 60 %; this reduction was not affected by 1 ± 10-7 g ml-1 BTX. BTX also reversibly decreased the mEPP frequency by 40 %, but not in the presence of CCh or in Ringer solution with 0 or 8 mM Ca2+. The present data show that BTX, which inhibits a class of nicotinic ACh receptors, does not block the decrease of mEPP frequency evoked by CCh and can itself suppress the frequency of spontaneous quantal release.

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