It works by blocking the function of acetylcholinesterase (AChE). Normally, when a motor neuron is stimulated, it releases the neurotransmitter acetylcholine (ACh) into the space between the neuron and an adjacent muscle cell, the synaptic cleft. When acetylcholine is taken up by the muscle cell, it stimulates muscle contraction. To avoid a state of constant muscle contraction, the acetylcholine is then broken down (hydrolysed) into the inactive substances acetic acid and choline by AChE. VX blocks the action of AChE, resulting in an accumulation of acetylcholine in the space between the neuron and muscle cell. On a molecular level, this leads to the ongoing stimulation and eventual fatigue of all affected muscarinic and nicotinic ACh receptors. This results in initial violent contractions, followed by "sustained supercontraction restricted to the fluid (sarcoplasm) of the subjunctional endplate and prolonged, depolarizing neuromuscular blockade." The prolonged blockade results in flaccid paralysis of all the muscles in the body, and it is such sustained paralysis of the diaphragm muscle that causes death by asphyxiation.