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acetylcholine (əsētˌəlkōˈlēn), a small organic molecule liberated at nerve endings as a neurotransmitter. It is particularly important in the stimulation of muscle tissue. The transmission of an impulse to the end of the nerve causes it to release neurotransmitter molecules onto the surface of the next cell, stimulating it. After such release, the acetylcholine is quickly broken into acetate and choline, which pass back to the first cell to be recycled into acetylcholine again. The poison curare acts by blocking the transmission of acetylcholine. Some nerve gases operate by preventing the breakdown of acetylcholine causing continual stimulation of the receptor cells, which leads to intense spasms of the muscles, including the heart. Acetylcholine is often abbreviated as Ach. See nervous system.
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A naturally occurring quaternary ammonium cation ester, with the formula CH3(O)COC2H4N(CH)3+, that plays a prominent role in nervous system function. The great importance of acetylcholine derives from its role as a neurotransmitter for cholinergic neurons, which innervate many tissues, including smooth muscle and skeletal muscle, the heart, ganglia, and glands. The effect of stimulating a cholinergic nerve, for example, the contraction of skeletal muscle or the slowing of the heartbeat, results from the release of acetylcholine from the nerve endings.

Acetylcholine is synthesized at axon endings from acetyl coenzyme A and choline by the enzyme choline acetyltransferase, and is stored at each ending in hundreds of thousands of membrane-enclosed synaptic vesicles. When a nerve impulse reaches an axon ending, voltage-gated calcium channels in the axonal membrane open and calcium, which is extremely low inside the cell, enters the nerve ending. The increase in calcium-ion concentration causes hundreds of synaptic vesicles to fuse with the cell membrane and expel acetylcholine into the synaptic cleft (exocytosis). The acetylcholine released at a neuromuscular junction binds reversibly to acetylcholine receptors in the muscle endplate membrane, a postsynaptic membrane that is separated from the nerve ending by a very short distance. The receptor is a cation channel which opens when two acetylcholine molecules are bound, allowing a sodium current to enter the muscle cell and depolarize the membrane. The resulting impulse indirectly causes the muscle to contract.

Acetylcholine must be rapidly removed from a synapse in order to restore it to its resting state. This is accomplished in part by diffusion but mainly by the enzyme acetylcholinesterase, which hydrolyzes acetylcholine.

Acetylcholinesterase is a very fast enzyme: one enzyme molecule can hydrolyze 10,000 molecules of acetylcholine in 1 s. Any substance that efficiently inhibits acetylcholinesterase will be extremely toxic.

McGraw-Hill Concise Encyclopedia of Bioscience. © 2002 by The McGraw-Hill Companies, Inc.
The following article is from The Great Soviet Encyclopedia (1979). It might be outdated or ideologically biased.



an acetic acid ester of choline: CH3COOCH2CH2N(CH3)3OH. Colorless crystals, readily soluble in water, alcohol, and chloroform; insoluble in ether. Its molecular weight is 163.2.

Acetylcholine is a biologically active substance widely distributed in nature. It is found in the tissues of organisms in small quantities (fractions of a microgram) in the form of an inactive compound with proteins and lipides; in certain pathological states, the acetylcholine content of the blood is increased. Acetylcholine in its active state is formed in the organism from acetic acid and choline under the action of the enzyme cholinacetylase; it is readily decomposed by enzymes of the cholinesterase group. Acetylcholine belongs to the group of mediators—transmitters of nerve stimuli in the peripheral and central nervous systems. It is secreted by the endings of the autonomic and motor nerve fibers and causes a specific reaction on the part of the innervating organ to stimulate a given nerve. Tiny sacs (vesicles) containing acetylcholine have been discovered in the presynaptic nerve endings. When a nerve is stimulated, acetylcholine enters the synaptic gap from these sacs; this effects transmission of the nerve impulse. When acetylcholine penetrates organs and tissues, it may cause effects characteristic of the excitation of the parasympathetic elements of the autonomic nervous system (lowering of blood pressure, slowing of heartbeat, increased peristalsis of stomach and intestines, pupilar contraction, and so on). The action of certain cholinesterase inhibitors (carbamates, organophosphorous insecticides, and certain poisonous substances) leads to the accumulation of excessive quantities of acetylcholine in the organism, which at first causes acceleration of nerve-impulse transmission (excitation) and later leads to termination of transmission—that is, the blocking of impulses (paralysis). Determination of acetylcholine is made principally by means of biological indicators—contraction of the spinal muscle in leeches and of the straight muscle of the abdomen in frogs, decrease in blood pressure in cats, and so on.


Fiziologicheskaia rol’ atsetilkholina i izyskanie novykh lekarstvennykh veshchestv Leningrad, 1957.
Al’pern, D. E. Kholinergicheskie protsessy ν patologii. Moscow, 1963.


The Great Soviet Encyclopedia, 3rd Edition (1970-1979). © 2010 The Gale Group, Inc. All rights reserved.


C7H17O3N A compound released from certain autonomic nerve endings which acts in the transmission of nerve impulses to excitable membranes.
McGraw-Hill Dictionary of Scientific & Technical Terms, 6E, Copyright © 2003 by The McGraw-Hill Companies, Inc.
References in periodicals archive ?
Sage extracts inhibit this same enzyme and boost acetylcholine levels.
Identification and localization of muscarinic acetylcholine receptor proteins in brain with subtype-specific antibodies.
One patient developed persistent atrial fibrillation with acetylcholine testing that was converted to sinus rhythm with intravenous amiodarone, without a night in the hospital.
Caption: Figure 5: Acetylcholine concentration in DRG tissues of sham stress group and water avoidance stress (WAS) group.
Kassiou, "PET radioligands for the vesicular acetylcholine transporter (VAChT)," Current Topics in Medicinal Chemistry, vol.
Finally, the time matched acetylcholine (100 [micro]M)-induced amplitude of contractions before and after exposure to atropine (10 [micro]M) of Hirschsprung's disease (H) were statistically compared with their corresponding values of non-Hirschsprung's cases (before values of H were compared with before values of NH and after values of H were compared with after values of NH).
While that seems like more good news, the reason for the enduring effect is not 100 percent clear: it could be the brain cells make more connections, it could be more acetylcholine keeps getting released, it could be both, the scientists note.
The sequences of primers were used in the polymerase chain reaction (PCR) using synthetic primers specific to choline acetyltransferase (ChAT), acetylcholine esterase (AChE), muscarinic acetylcholine receptors (Mj mAChR and [M.sub.2] mAChR), and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as follows:
About 95% of serotonin is released in the gastrointestinal tract in response to release of acetylcholine.2,3 So acetylcholine and serotonin-mediated intestinal activity was taken as the control.4
The compounds used for preincubation were: i) the vehicle (distilled water); ii) [10.sup.-6] M atropine, a competitive muscarinic acetylcholine receptor antagonist; iii) [10.sup.v5] M L-NAME, a direct inhibitor of NO synthase; iv) [10.sup.-2] M TEA, a [Ca.sup.2+]-activated K+ channel blocker and nonspecific voltage-activated [K.sup.+] channel blocker; v) [10.sup.-3] M 4-aminopyridine (4-AP), a voltage-activated [K.sup.+] channel blocker; vi) 3.1 x [10.sup.-7] M glibenclamide, an ATP-sensitive [K.sup.+] channel blocker, (KATP); vii) [10.sup.-5] M indomethacin, a prostaglandin synthesis inhibitor; viii) [10.sup.-5] M clotrimazole, a cytochrome P450 inhibitor; and ix) [10.sup.-5] M cycloheximide, a general protein synthesis inhibitor.
apple juice, theorized to increase acetylcholine levels; and
Nicotine mimics the actions of a natural chemical messenger, acetylcholine, which stimulates the receptors for nicotine in the brain.