Why does a drug that inhibits acetylcholinesterase at the neuromuscular junction cause sustained muscle contraction, rather than a normal cycle of contraction and relaxation?

💡 Explanation

Acetylcholinesterase normally breaks down acetylcholine, terminating receptor activation. Because the drug inhibits this enzyme, acetylcholine remains in the synaptic cleft longer, therefore prolonging postsynaptic receptor activation and leading to sustained contraction, rather than rapid clearance.

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