The enzyme cholinesterase (EC 3.1.1.8, choline esterase; systematic name acylcholine acylhydrolase) catalyses the hydrolysis of choline-based esters: Several of these serve as neurotransmitters.

But such usage is now outdated; the current, unambiguous HGNC names and symbols are acetylcholinesterase (ACHE) and butyrylcholinesterase (BCHE).

[5][6] In 1968, Walo Leuzinger et al. successfully purified and crystallized acetylcholinesterase from electric eels at Columbia University, New York.

This is a silent condition that manifests itself only when people that have the deficiency receive the muscle relaxants succinylcholine or mivacurium during a surgery.

[10] Some early research points to genetic butylcholinesterase deficiency as a possible candidate component in sudden infant death syndrome.

By injecting a mouse with acetylcholin esterase inhibitors and electrical stimulation, the muscle develops trigger points.

Because of its essential function, chemicals that interfere with the action of cholinesterase are potent neurotoxins, causing excessive salivation and eye-watering in low doses, followed by muscle spasms and ultimately death (examples are some snake venoms, and the nerve gases sarin and VX).

The so-called nerve gases and many substances used in insecticides have been shown to act by combining with a residue of serine in the active site of acetylcholine esterase, inhibiting the enzyme completely.

[17] Outside of biochemical warfare, anticholinesterases are also used for reversing medication induced paralysis during anesthesia; as well as in the treatment of myasthenia gravis, glaucoma, and Alzheimer's disease.