The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the NMJ, action potential arises, and impulse transmission across the NMJ facilitates skeletal muscle contractions.

As the nerve impulse arrives at the synaptic bulb ends, it stimulates Ca²⁺ influx by opening the calcium channels, which stimulates exocytosis of the synaptic vesicles and release of acetylcholine in the synaptic cleft. Two acetylcholine molecules bind to the receptor at the motor end plate, opening Na⁺ channels. Na⁺ influx inside the muscle fiber changes the membrane potential, triggering a muscle action potential followed by muscle contraction. The effect of acetylcholine is brief as the enzyme acetylcholinesterase breaks down acetylcholine into choline and acetate.

Certain agents can block the events at the NMJ to prevent muscle contraction. Botulinum toxin prevents exocytosis of the synaptic vesicles, preventing acetylcholine release. Tubocurarine and other neuromuscular blockers can limit impulse transmission across the NMJ by binding to acetylcholine receptors. This is important for treating several pathological conditions and for use during patient surgeries to induce muscle relaxation and temporary paralysis.