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Acetylcholinesterase is an enzyme that hydrolyses the neurotransmitter acetylcholine to choline and acetate. Its activity helps terminate signalling at cholinergic synapses, including the neuromuscular junction. Chemically, it is a catalyst: the reaction consumes acetylcholine and water, while the enzyme can be reused.^[ref]

The distinction between removal of a messenger and inhibition of its receptor matters. Reducing acetylcholinesterase activity leaves more acetylcholine available to activate receptors; it does not directly substitute for the messenger or block every receptor. Thus the duration of a chemical signal depends both on its release and on its clearance. Measuring reaction-product accumulation in an enzyme assay tests the clearance machinery separately from a responding muscle or neuron.

A cholinergic synapse is a chemical synapse that uses acetylcholine as a neurotransmitter. Release of acetylcholine allows it to bind receptors on the receiving cell. The response depends on receptor type: a nicotinic acetylcholine receptor is an ion channel, whereas a muscarinic acetylcholine receptor signals through a G protein.^[ref]

At a neuromuscular junction, activation of nicotinic acetylcholine receptors helps trigger a skeletal-muscle action potential. Other cholinergic pathways can change a cell's activity more slowly through muscarinic acetylcholine receptors. Thus naming the transmitter does not completely specify the postsynaptic effect. Acetylcholinesterase helps terminate signaling by breaking down acetylcholine in the synaptic region.^[ref]

A motor neuron is a neuron whose output drives or regulates an effector, commonly muscle. A somatic motor neuron carries action potentials along its axon to a neuromuscular junction, where release of acetylcholine promotes excitation of a muscle fibre. Neural excitation, transmitter release and muscle force are successive steps. ^[ref]

A reflex illustrates the distinction between a sensory input and a motor output: a circuit converts an incoming signal into activity of an efferent neuron. The number and timing of motor-neuron impulses can change force without changing the identity of the contacted muscle. Clinical distinctions between upper and lower motor neurons refer to different positions in a motor pathway, so not every neuron involved in motor control directly innervates muscle.

A neuromuscular junction is the specialized synapse through which a somatic motor neuron excites a skeletal muscle fibre. Arrival of an action potential at the nerve terminal opens voltage-gated calcium channels; calcium entry triggers release of acetylcholine. Binding of acetylcholine to receptors on the muscle's motor end plate produces a local depolarization that normally triggers a muscle action potential.^[ref]

The electrical signal then initiates release of stored calcium within the muscle fibre, enabling contraction. Synaptic release and contraction are separate steps: the acetylcholine does not itself pull the contractile filaments. Breakdown of acetylcholine by acetylcholinesterase helps terminate the synaptic signal.^[ref]