What Is the Function of Acetylcholine?
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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.
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)
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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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.