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.