Which agent is a depolarizing NMJ blocker?

Prepare for the INBDE Pharmacology Test with flashcards and multiple-choice questions, each question has hints and explanations. Get ready for your exam!

Multiple Choice

Which agent is a depolarizing NMJ blocker?

Explanation:
Depolarizing NMJ blockers work by briefly activating the nicotinic acetylcholine receptors at the motor endplate, causing an initial depolarization with fasciculations, then desensitization of the receptor that prevents further transmission and leads to paralysis. Succinylcholine is the classic example because it binds to those receptors like acetylcholine and remains at the receptor long enough to keep the channel depolarized, producing a short-lived yet reliable paralysis. Its effect is due to this persistent receptor activation and subsequent desensitization, not by simply blocking acetylcholine binding. In contrast, agents like D-tubocurarine are nondepolarizing because they competitively block the receptor without causing initial depolarization, and cholinesterase inhibitors such as physostigmine and neostigmine increase acetylcholine levels to enhance NMJ transmission or reverse nondepolarizing blocks, not to depolarize the endplate.

Depolarizing NMJ blockers work by briefly activating the nicotinic acetylcholine receptors at the motor endplate, causing an initial depolarization with fasciculations, then desensitization of the receptor that prevents further transmission and leads to paralysis. Succinylcholine is the classic example because it binds to those receptors like acetylcholine and remains at the receptor long enough to keep the channel depolarized, producing a short-lived yet reliable paralysis. Its effect is due to this persistent receptor activation and subsequent desensitization, not by simply blocking acetylcholine binding. In contrast, agents like D-tubocurarine are nondepolarizing because they competitively block the receptor without causing initial depolarization, and cholinesterase inhibitors such as physostigmine and neostigmine increase acetylcholine levels to enhance NMJ transmission or reverse nondepolarizing blocks, not to depolarize the endplate.

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