Which agent is a non-depolarizing NMJ blocker?

Which agent is a non-depolarizing NMJ blocker?

• A. D-Tubocurarine
• B. Succinylcholine
• C. Physostigmine
• D. Neostigmine

Answer: (A)

Non-depolarizing NMJ blockers work by acting as competitive antagonists at the nicotinic acetylcholine receptors at the motor end plate. They prevent acetylcholine from binding and triggering depolarization, so the muscle cannot contract. Because their effect is competitive, increasing acetylcholine at the junction can outcompete the blocker and restore function, which is why acetylcholinesterase inhibitors can reverse their effect. D-tubocurarine is a classic example of this type of blocker, binding to the nicotinic receptors and blocking ACh-induced depolarization without causing an initial depolarization itself. Succinylcholine, in contrast, is a depolarizing NMJ blocker; it acts as an acetylcholine receptor agonist, causing brief depolarization and fasciculations before desensitizing the receptor and producing flaccid paralysis. Acetylcholinesterase inhibitors like physostigmine and neostigmine raise acetylcholine levels but are not NMJ blockers themselves; they are used to reverse non-depolarizing block by increasing ACh at the end plate.

Non-depolarizing NMJ blockers work by acting as competitive antagonists at the nicotinic acetylcholine receptors at the motor end plate. They prevent acetylcholine from binding and triggering depolarization, so the muscle cannot contract. Because their effect is competitive, increasing acetylcholine at the junction can outcompete the blocker and restore function, which is why acetylcholinesterase inhibitors can reverse their effect.

D-tubocurarine is a classic example of this type of blocker, binding to the nicotinic receptors and blocking ACh-induced depolarization without causing an initial depolarization itself. Succinylcholine, in contrast, is a depolarizing NMJ blocker; it acts as an acetylcholine receptor agonist, causing brief depolarization and fasciculations before desensitizing the receptor and producing flaccid paralysis. Acetylcholinesterase inhibitors like physostigmine and neostigmine raise acetylcholine levels but are not NMJ blockers themselves; they are used to reverse non-depolarizing block by increasing ACh at the end plate.