Abstract
Summary.: The repolarization of the end‐plate region and the neuromuscular block caused in frog skeletal muscle by persisting high concentrations of acetylcholine could be due either to a niechanisni rrducing the reactivity of the end‐plate “receptors” without affecting the membrane. i. e. a tubocurarine‐like effect. or to the possibility that the membrane at the end‐plate region was left highly permeable to ions other than sodium.To determine which of these two alternative iriechanisms is lrsponsible for the effects of persisting concentrations of acctylcholine, determinations were made of the transverse electric. membrane resistance at the end‐plate region heforc and after the application of acetylcholine.It was shown that the transverse membrane resistance was completely normal when acetylcholine had caused a neuromuscular block and the end‐plate region was repolarized.This excludes the possibility that the repolarization of the end‐plate region with the neuromuscular block in the presence of persisting concentrations of acetylcholine is due to an increase in the ionic permeability of the muscle membrane. It is concluded that the only other known mode of action which could account for these effects of acetylcholine is that exerted hp tubocurarine.