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What Is the Function of Acetylcholine?

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Acetylcholine, an ester of choline and acetic acid that serves as a transmitter substance of nerve impulses within the central and peripheral nervous systems. Acetylcholine is the chief neurotransmitter of the parasympathetic nervous system, the part of the autonomic nervous system (a branch of the peripheral nervous system) that contracts smooth muscles, dilates blood vessels, increases bodily secretions, and slows heart rate. Acetylcholine can stimulate a response or block a response and thus can have excitatory or inhibitory effects.

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ACh is synthesized by a single step reaction catalyzed by the biosynthetic enzyme choline acetyltransferase. As is the case for all nerve terminal proteins, CAT is produced in the cholinergic cell body and transported down the axon to the nerve endings. Both CAT and ACh may be found throughout the neuron, but their highest concentration is in axon terminals. The presence of CAT is the "marker" that a neuron is cholinergic, only cholinergic neurons contain CAT. The rate-limiting steps in ACh synthesis are the availability of choline and acetyl-CoA. During increased neuronal activity the availability of acetyl-CoA from the mitochondria is upregulated as is the uptake of choline into the nerve ending from the synaptic cleft

Ca2+ appears to be involved in both of these regulatory mechanisms. As will be described later, the inactivation of ACh is converted by metabolism to choline and acetic acid. Consequently much of the choline used for ACh synthesis comes from the recycling of choline from metabolized ACh. Another source is the breakdown of the phospholipid, phosphatidylcholine. One of the strategies to increase ACh neurotransmission is the administration of choline in the diet. However, this has not been effective, probably because the administration of choline does not increase the availability of choline in the CNS. The NMJ nicotinic ACh receptor consists of five polypeptide subunits: two α subunits and one each of β, δ, and γ (see Figure 11.8). A funnel-shaped internal ion channel is surrounded by the five subunits. The binding surface of the receptor appears to be primarily on the α subunits, near the outer surface of the molecule. The subunits contain recognition sites for agonists, reversible antagonists, and α-toxins (cobra α-toxin and α-bungarotoxin). Whereas the NMJ nicotinic receptor is composed of four different species of subunit (2 α, β, γ, δ), the neuronal nicotinic receptor also is composed of only two subunit types (2 α and 3 β). Muscarinic receptors, classified as G protein coupled receptors (GPCR), are located at parasympathetic autonomically innervated visceral organs, on the sweat glands and piloerector muscles and both post-synaptically and pre-synaptically in the CNS (see Table I). The muscarinic receptor is composed of a single polypeptide. Seven regions of the polypeptide are made up of 20-25 amino acids arranged in an α helix. Because each of these regions of the protein is markedly hydrophobic, they span the cell membrane seven times. The fifth internal loop and the carboxyl-terminal tail of the polypeptide receptor are believed to be the site of the interaction of the muscarinic receptor with G proteins (see right). The site of agonist binding is a circular pocket formed by the upper portions of the seven membrane-spanning regions.

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The seminal paper on the actions of acetylcholine was that of Dale (1914). This arose from his work at the Wellcome Physiological (not Pharmacological!) Research Laboratories, on extracts of ergot. Eight years earlier, Hunt & Taveau had reported the strong vasodepressor action of acetylcholine, and the ergot extract produced a similar effect. Dale and his colleagues thought the extract might contain muscarine (at that time not identified chemically), but the active principle, isolated by A.J. Ewins in the same year, turned out to be acetylcholine. In this paper, Dale compared the effects of acetylcholine with choline and with various other esters and ethers of choline, and came to the key division into ‘muscarine' and ‘nicotine' effects. It is clear that the discovery of acetylcholine in the body was, for Dale, the ‘clincher' for its putative neurotransmitter function. Immediately thereafter, there appeared an avalanche of papers from Dale's laboratory at the National Institute for Medical Research, published (primarily in the Journal of Physiology) with a number of colleagues who dominated U.K. pharmacology over the subsequent years (DALE H.H., 1914). Between 1934 and 1936, Dale, Feldberg and collaborators established a role for acetylcholine as a neurotransmitter from the vagus nerve to the stomach, from sympathetic nerves to sweat glands (which Dale had earlier suggested might be anomalously cholinergic), and at the skeletal neuromuscular junction. In the interim (and as a clear prelude to the work on skeletal muscle), W

Feldberg and his colleagues – initially in Berlin but subsequently at the National Institute – established the cholinergic nature of transmission from preganglionic sympathetic nerves to the adrenal medulla and to the sympathetic ganglion. The first reasonably definitive evidence for a localized transmitter function came from Eccles et al. (1956), after his Pauline conversion from electrical to chemical transmission (ADAMS P.R., BROWN D.A., 1982)

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Obviously, the venom of a black widow spider acts by causing the release of acetylcholine. When a person is bitten by a black widow, their acetylcholine levels rise dramatically, leading to severe muscle contractions, spasms, paralysis, and even death

Acetylcholine is a critical neurotransmitter that plays an important role in the normal function of the brain and body. Disruptions in the release and function of this neurotransmitter can result in significant problems in areas such as memory and movement

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Pharmacological investigations on a central synapse operated by acetylcholine. ECCLES JC, ECCLES DM, FATT P J Physiol. 1956 Jan 27; 131(1):154-69.

Release from brain tissue of compounds with possible transmitter function: interaction of drugs with these substances. Vogt M Br J Pharmacol. 1969 Oct; 3 7(2):325-37.

DALE H.H. The action of certain esters and ethers of choline, and their relation to muscarine. J. Pharmacol. Exp. Ther. 1914;6:147–190.

ADAMS P.R., BROWN D.A. Synaptic inhibition of the M-current: slow excitatory post-synaptic potential mechanism in bullfrog sympathetic neurones. J. Physiol. 1982;332:263–272.

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