Depolarizing neuromuscular block--a presynaptic mechanism?

Abstract

It has been known since 1951 that drugs such as decamethonium and suxamethonium produced an acetylcholine like (agonist) effect on the postsynaptic membrane of the neuromuscular junction causing depolarization. Inspite of evidence of action of these drugs on the motor nerve terminals, it has been widely assumed that the neuromuscular block they produced is the result of depolarization followed by desensitization of the postsynaptic membrane. Evidence questioning the view that these drugs produce their clinical effects as a consequence of depolarization of the postsynaptic membrane or desensitization is presented together with the results of recent experiments which are more readily explained by proposing a presynaptic action of these drugs, initially stimulating then depressing acetylcholine release.