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When a nerve impulse reaches an axon ending, voltage-gated calcium channels in the axonal membrane open and calcium, which is extremely low inside the cell, enters the nerve ending. The increase in calcium-ion concentration causes hundreds of synaptic vesicles to fuse with the cell membrane and expel acetylcholine into the synaptic cleft (exocytosis). The acetylcholine released at a neuromuscular junction binds reversibly to acetylcholine receptors in the muscle end-plate membrane, a postsynaptic membrane that is separated from the nerve ending by a very short distance. The receptor is a cation channel which opens when two acetylcholine molecules are bound, allowing a sodium current to enter the muscle cell and depolarize the membrane. The resulting impulse indirectly causes the muscle to contract.

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