DEMO DEMOPharmacology Of Neuromuscular Transmission
Drugs can block neuromuscular transmission either by inhibiting the synthesis and/or release of acetylcholine from motor nerve terminals or by interfering with the postsynaptic actions of acetylcholine. All clinically useful agents have their primary action at the motor end plate and are conveniently classified into:
The mechanisms by which agents in these groups block neuromuscular transmission differ. Non-depolarizing drugs block nicotinic cholinoceptors of the endplate in a competitive, reversible manner. It is unlikely that their actions in blocking the end plate channels and possible pre-junctional inhibition of acetylcholine release is of practical significance. Depolarizing blockers, by prolonged stimulation of the nicotinic cholinoceptors, cause a persistent depolarization of the endplate with a consequent loss of excitability together with an inactivation of surrounding voltage-gated sodium channels (i.e. they no longer open in response to a depolarizing stimulus). The acute antagonism of neuromuscular transmission by depolarizing blocking agents is usually referred to as Phase I and is illustrated in experiments 1-7 in the program. On repeated administration of these drugs the characteristics of the block change (Phase II) and are illustrated in experiment 8.
Because the mechanisms of action of the two groups of drugs differ, the characteristics of the block of neuromuscular transmission also differ. The results of the experiments presented here illustrate such differences.
