Depolarizing neuromuscular block--a presynaptic mechanism?
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.
Magill Department of Anaesthetics, Charing Cross and Westminster Medical School, London, U.K.
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S
Feldman
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J
Hood
D000818:Animals; D006801:Humans; D009045:Motor Endplate / Q000187:drug effects; D009046:Motor Neurons / Q000187:drug effects; D009411:Nerve Endings / Q000187:drug effects; D009467:Neuromuscular Depolarizing Agents / Q000494:pharmacology*; D009469:Neuromuscular Junction / Q000187:drug effects; D017729:Presynaptic Terminals / Q000187:drug effects*; D013569:Synapses / Q000187:drug effects
D009467:Neuromuscular Depolarizing Agents