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Nerves connect with muscles at the neuromuscular junction. There, the ends of nerve fibers connect to special sites on the muscle's membrane called motor end plates. These plates contain receptors that enable the muscle to respond to acetylcholine, a chemical messenger (neurotransmitter) released by the nerve to transmit a nerve impulse across the neuromuscular junction. After a nerve stimulates a muscle at this junction, an electrical impulse flows through the muscle, causing it to contract. After transmitting the impulse, acetylcholine is broken down so that it does not continue to stimulate the muscle.
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Disorders in which the neuromuscular junction malfunctions include myasthenia gravis (see Peripheral Nerve Disorders: Myasthenia Gravis ), botulism (see Peripheral Nerve Disorders: Botulism), and Eaton-Lambert syndrome (see Peripheral Nerve Disorders: Eaton-Lambert Syndrome). In addition, many drugs (including very high doses of some antibiotics), certain insecticides (organophosphates), curare (an extract from plants formerly placed on the tip of some poison darts and used to paralyze and kill), and the nerve gases used in chemical warfare can cause the neuromuscular junction to malfunction. Some of these substances prevent the normal breakdown of acetylcholine after the nerve impulse has been transmitted to the muscle.
Last full review/revision September 2012 by Michael Rubin, MDCM
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