Neuropharmacology Vol 32, No. 2, pp. 169-174, 1993
E. GHANSAH, P. KoPSOMBUT, M.A. MALEQUE and A. B Ross
Mescaline (3.4,5-trimethoxyphenylethylamine; MES) and its analogs, anhalinine (ANH) and methylenemescaline trimer (MMT) were investigated, using sciatic-sartonus preparations of the frog and cortical tissue from the rat. The effects of MES and its analogs were examined with respect to muscle twitch, restmg membrane potential and nicotinic receptor binding. Mescaline and its analogs (10-100 µM) blocked both directly and neurally evoked twitches but their effects on neurally evoked twitches were greater than those on directly evoked twitches. Mescaline, ANH and MMT decreased amplitude of the miniature endplate and endplate potentials, decreased acetylcholine (ACh) quanta! content, hyperpolarized the resting membrane potential and prolonged duratt0n of the action potential. They did not significantly displace the binding of (1251)-ix-bungarotoxin (ix-BTX) to nicotinic receptors, at concentrations which blocked neuromuscular transmission. These results suggest that MES and its analogs inhibit cholinergic neuromuscular transmission by blocking release of ACh; they also affect K+ conductance.
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EFFECTS OF MESCALINE AND SOME OF ITS ANALOGS ON CHOLINERGIC NEUROMUSCULAR TRANSMISSION
Mescaline and its analogs inhibit cholinergic neurotransmission at the neuromuscular junction