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Neuromuscular junction

A neuromuscular junction is a chemical synapse formed by the contact between a motor neuron and a muscle fiber. It is the site in which a motor neuron transmits a signal to a muscle fiber to initiate muscle contraction. The sequence of events that results in the depolarization of the muscle fiber at the neuromuscular junction begins when an action potential is initiated in the cell body of a motor neuron, which is then propagated by saltatory conduction along its axon toward the neuromuscular junction. Once it reaches the terminal bouton, the action potential causes a Ca ion influx into the terminal by way of the voltage-gated calcium channels. The Ca influx causes synaptic vesicles containing the neurotransmitter acetylcholine to fuse with the plasma membrane, releasing acetylcholine into the synaptic cleft between the motor neuron terminal and the neuromuscular junction of the skeletal muscle fiber. Acetylcholine diffuses across the synapse and binds to and activates nicotinic acetylcholine receptors on the neuromuscular junction. Activation of the nicotinic receptor opens its intrinsic sodium / potassium channel, causing sodium to rush in and potassium to trickle out. As a result, the sarcolemma reverses polarity and its voltage quickly jumps from the resting membrane potential of -90mV to as high as +75mV as sodium enters. The membrane potential then becomes hyperpolarized when potassium exits and is then adjusted back to the resting membrane potential. This rapid fluctuation is called the end-plate potential. The voltage-gated ion channels of the sarcolemma next to the end plate open in response to the end plate potential. They are sodium and potassium specific and only allow one through. This wave of ion movements creates the action potential that spreads from the motor end plate in all directions. If action potentials stop arriving, then acetylcholine ceases to be released from the terminal bouton. The remaining acetylcholine in the synaptic cleft is either degraded by active acetylcholine esterase or reabsorbed by the synaptic knob and none is left to replace the degraded acetylcholine.