Abstract

Summary. The neuromuscular block produced in frog muscle by acetylcholine, nicotine, decamethonium and succinylcholine has been investigated with extracellular and intracellular recording electrodes. The agents investigated are found to act on the neuromuscular junction in a qualitatively similar way. They cause a brief depolarization of the end‐plate regions, which nevertheless subsides spontaneously without removal of the agents, and restoration of the membrane potential to about its normal value takes place. A neuromuscular block develops during the phase of depolarization and persists despite repolarization of the muscle membrane. The period of depolarization is not accompanied by a maximum of neuromuscular block, and a complete neuromuscular block does not develop until the membrane potential of the end‐plate regions is restored to about its normal value. During the block of neuromuscular transmission, the end‐plate regions of the muscle are insensitive to the depolarizing effect of the transmitter substance. It is concluded that the neuromuscular block caused by acetyl‐choline, nicotine, decamethonium and succinylcholine is not due to a persistent depolarization of the end‐plate regions or of adjacent muscle membrane, but to a decrease in sensitivity of the end‐plate to the transmitter substance. The effects of the agents on the time‐course of the end‐plate potential and on the electrical threshold of the muscle membrane have been investigated. The results and their implications are discussed with reference to existing theories on the mode of neuromuscular block caused by the agents investigated.