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Decamethonium, which has a short action time, is similar to acetylcholine and acts as a partial agonist of the nicotinic acetylcholine receptor. In the motor endplate, it causes depolarization, preventing further effects to the normal release of acetylcholine from the presynaptic terminal, and therefore preventing the neural stimulus from affecting the muscle. In the process of binding, decamethonium activates (depolarizes) the motor endplate - but since the decamethonium itself is not degraded, the membrane remains depolarized and unresponsive to normal acetylcholine release.
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