Acetylcholine is released at the neuromuscular junction to trigger skeletal muscle contraction.
A motor neuron carries an electrical signal to the nerve ending beside a skeletal muscle fiber. The arrival of that signal opens calcium channels, causing synaptic vesicles to release acetylcholine into the tiny gap between nerve and muscle, called the neuromuscular junction.
Acetylcholine binds to nicotinic acetylcholine receptors on the muscle membrane. This produces an electrical change that initiates an action potential in the muscle fiber and ultimately leads to contraction. The enzyme acetylcholinesterase then breaks down acetylcholine, helping end the signal and allowing precise control.
Acetylcholine also acts in the brain and in the autonomic nervous system, so it is not exclusively a muscle messenger. A well-known medical example is myasthenia gravis, in which antibodies disrupt communication at neuromuscular junctions and cause weakness. Botulinum toxin prevents acetylcholine release at these junctions, producing temporary muscle paralysis.