Acetylcholine (redirected from Acetylcholine receptors)

acetylcholine (əsēt'əlkō`lēn), 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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acetylcholine

Ester of choline and acetic acid, a neurotransmitter active at many nerve synapses and at the motor end plate of vertebrate voluntary muscles. It affects several of the body's systems, including the cardiovascular system (decreases heart rate and contraction strength, dilates blood vessels), gastrointestinal system (increases peristalsis in the stomach and amplitude of digestive contractions), and urinary system (decreases bladder capacity, increases voluntary voiding pressure). It also affects the respiratory system and stimulates secretion by all glands that receive parasympathetic nerve impulses (see autonomic nervous system). It is important in memory and learning and is deficient in the brains of those with late-stage Alzheimer disease.

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Acetylcholine

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.