Neuromuscular junction

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Image:NMJ.jpg A neuromuscular junction is the synapse or junction of the axon terminal of a motoneuron with the motor end plate, the highly-excitable region of muscle fiber plasma membrane responsible for initiation of action potentials across the muscle's surface, ultimately causing the muscle to contract. The signal passes through the neuromusclar junction via the neurotransmitter acetylcholine.

1 Anatomy
2 Mechanism of Action
3 Neuromuscular junction disorders
4 See also
5 Sources

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Anatomy

Motor neuron (efferent) axons originating in the spinal cord contact muscle fibers via a structure known as the motor endplate. Here, motor neuron axons lose their myelin sheath and branch into multiple endings, which occupy depressions in the sarcolemma. Motor neurons can innervate from one to over 100 muscle fibers, but each muscle fiber receives only inputs from only one motor neuron. In the terminal branches of the motor nerve, structures known as presynaptic active zones accumulate synaptic vesicles filled with the neurotransmitter acetylcholine. On the muscle side of the junction, the muscle fiber is folded into grooves called postjunctional folds that mirror the presynaptic active zones, the spaces between the folds contain acetylcholine receptors. The muscle surface is covered by the synaptic basal lamina. Postjunctional folds are characteristic of skeletal muscle, particularily in fast muscle fibers.

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Mechanism of Action

Upon the arrival of an action potential at the axon terminal, calcium ions flow from the extracellular fluid into the motoneuron's cytosol and trigger a biochemical cascade that causes neurotransmitter-containing vesicles to fuse to the motoneuron's cell membrane and thus release acetylcholine into the synaptic cleft. Acetylcholine then binds to the nicotinic acetlycholine receptors that dot the motor end plate. The receptors are ion channels, and when bound by acetylcholine, they open, allowing sodium and potassium ions to flow in and out of the muscle's cytosol, respectively. Because of the differences in electrochemical gradients across the plasma membrane, more sodium moves in than potassium out, producing a local depolarization of the motor end plate known as an end plate potential (EPP). This depolarization spreads across the surface of the muscle fiber into transverse tubules, eliciting the release of calcium from the sarcoplasmic reticulum, thus initiating muscle contraction. The action of acetlycholine is terminated when the enzyme acetylcholinesterase degrades the neurotransmitter.

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