Summary
Highlights
The neuromuscular junction is where a motor neuron communicates with skeletal muscle to initiate contraction. The signal transmission involves an electrical signal, converted to a chemical signal, and then back to an electrical signal in the muscle.
An action potential, involving the opening of voltage-gated sodium channels, propagates down the neuron. Sodium influx makes the inside of the membrane positive, triggering the opening of the next channel in a domino effect.
At the neuron's end, the charge change opens voltage-gated calcium channels. Influx of calcium causes vesicles filled with the neurotransmitter acetylcholine (ACh) to fuse with the membrane and release ACh into the synaptic space.
Acetylcholine diffuses across the synapse and binds to nicotinic acetylcholine receptors on the muscle membrane. These are ligand-gated sodium channels, and their opening leads to sodium influx, depolarizing the muscle membrane.
The depolarization spreads deep into the muscle via T-tubules, triggering the sarcoplasmic reticulum to release stored calcium. Calcium is essential for muscle contraction, as it unlocks binding sites on actin, allowing myosin heads to pull on the actin filaments, causing muscle shortening (with ATP).
Acetylcholine has only about 1 millisecond to bind to its receptors before it is broken down by acetylcholinesterase in the synapse. This enzyme ensures rapid muscle relaxation and allows the system to reset for the next impulse.
Depolarizing muscle relaxants, like succinylcholine, mimic acetylcholine but last longer, causing initial contractions (fasciculations) followed by flaccid paralysis because the muscle membrane remains depolarized and cannot reset. Nondepolarizing relaxants block acetylcholine receptors, preventing depolarization and contraction. Their effects can be reversed by inhibiting acetylcholinesterase, allowing endogenous acetylcholine to compete and bind.