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When the neurotransmitter acetylcholine is applied to skeletal muscle cells, it binds the acetylcholine receptor and causes the muscle cells to contract. Succinylcholine, which is a chemical analog of acetylcholine, binds to the acetylcholine receptor on skeletal muscle cells but causes the muscle cells to relax; it is therefore often used by surgeons as a muscle relaxant. Propose a model for why succinylcholine causes muscle relaxation. What might be the mechanism to explain the different activities of acetylcholine and succinylcholine on the acetylcholine receptor?

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Answer & explanation:

Succinylcholine is a depolarizing neuromuscular blocker, these substances bind to the nicotinic receptor and act as acetylcholine, depolarizing the neuromuscular junction.

However, unlike acetylcholine, which is instantly destroyed by acetylcholinesterase, depolarizing blockers persist in high concentration in the synaptic cleft, remaining bound to the receptor for a relatively longer time and causing constant receptor stimulation.

This mechanism causes the opening in sodium (Na⁺) channels, producing transient fasciculations and flaccid paralysis. After that, the membrane repolarizes, but the receptor is resuscitated by the effect of acetylcholine.

The difference in mechanisms is precisely due to the fact that acetylcholine is rapidly degraded (as a result of acetylcholinesterase), while succinylcholine persists for a relatively longer time to the receptor due to its high concentration in synaptic clefts.

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