Function of the Neuromuscular Junction

A neuromuscular junction (NMJ) 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. In vertebrates, the signal passes through the neuromuscular junction via the neurotransmitter acetylcholine.


Anatomy
When a motor neuron enters a muscle, it loses its myelin sheath and splits into many terminal branches. Motor neuron (efferent) axons originating in the spinal cord enter muscle fibers, where they split into many unmyelinated branches. These terminal fibers run along the myocytes to end at the neuromuscular junction, which occupies a depression in the sarcolemma. Each motor neuron can innervate from one to over 2000 muscle fibers, but each muscle fiber receives inputs from only one motor neuron.

In the terminal bouton 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, particularly in fast muscle fibers.
Mechanism of action
Upon the arrival of an action potential at the axon terminal, voltage-dependent calcium channels open and Ca2+ ions flow from the extracellular fluid into the motor neuron's cytosol. This influx of Ca2+ triggers excitation-contraction coupling, a biochemical cascade that causes neurotransmitter-containing vesicles to fuse to the motor neuron's cell membrane and release acetylcholine into the synaptic cleft.

Acetylcholine diffuses across the synaptic cleft and binds to the nicotinic acetylcholine receptors that dot the motor end plate.

The receptors are ligand-gated 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 acetylcholine is terminated when the enzyme acetylcholinesterase degrades the neurotransmitter and the unhydrolysed neurotransmitter diffuses away.

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