Acetylcholine receptors Acetyltransferase

Khan, W.A., Dechkovskaia, A.M., Herrick, E.A., Jones, K.H., Abou-Donia, M.B. (2000). Acute sarin exposure causes differential regulation of choline acetyltransferase, acetylcholinesterase, and acetylcholine receptors in the central nervous system of the rat. Toxicol. Sci. 57 112-20. 

Catalpol. Zhang et al. [233] studied the neuroprotective effects of catalpol, an iridoid glycoside isolated from the fresh rehmannia roots, on the cholinergic system and inflammatory cytokines in the senescent mouse brain induced by D-galactose. Acetylcholinesterase (AChE) activity increased in senescent mouse brain and choline acetyltransferase (ChAT) decreased in the basal forebrain of senescent mouse. Muscarinic acetylcholine receptor Ml (mAChRl) expression declined and the levels of tumor necrosis factor (TNF-a), interleukin-ip (IL-ip), and advanced glycation end products... 

Acetylcholine is synthesized from choline and acetyl-CoA, by choline acetyltransferase, in the axonal terminal bulbs of nerve cells. After acetylcholine has been released from vesicles and bound to the receptors, the neurotransmitter is rapidly hydrolyzed by the enzyme acetylcholinesterase, yielding choline, which binds poorly to acetylcholine receptors. Degradation of acetylcholine restores the resting potential in the postsynaptic membrane. After it has been released from vesicles and bound to the receptors, the neurotransmitter is rapidly hydrolyzed by the enzyme acetylcholinesterase, yielding choline, which binds poorly to acetylcholine receptors. Degradation of acetylcholine restores the resting potential in the postsynaptic membrane. 

Michalek, H., Fortuna, S., Volpe, M.T., et al., 1990. Age-related differences in the recovery rate of brain cholinesterases, choline acetyltransferase and muscarinic acetylcholine receptor sites after a subacute intoxication of rats with the anticholinesterase agent, isofluorophate. Acta Neurobiol. Exp. (Wars)... 

Acetylcholine. Acetylcholiae (ACh) (1) is a crystalliae material that is very soluble ia water and alcohol. ACh, synthesized by the enzyme choline acetyltransferase (3), iateracts with two main classes of receptor ia mammals muscarinic (mAChR), defiaed oa the basis of the agonist activity of the alkaloid muscarine (4), and nicotinic (nAChR), based on the agonist activity of nicotine (5) (Table 1). m AChRs are GPCRs (21) n AChRs are LGICs (22). 

Schematic illustration of a generalized cholinergic junction (not to scale). Choline is transported into the presynaptic nerve terminal by a sodium-dependent choline transporter (CHT). This transporter can be inhibited by hemicholinium drugs. In the cytoplasm, acetylcholine is synthesized from choline and acetyl -A (AcCoA) by the enzyme choline acetyltransferase (ChAT). Acetylcholine is then transported into the storage vesicle by a second carrier, the vesicle-associated transporter (VAT), which can be inhibited by vesamicol. Peptides (P), adenosine triphosphate (ATP), and proteoglycan are also stored in the vesicle. Release of transmitter occurs when voltage-sensitive calcium channels in the terminal membrane are opened, allowing an influx of calcium. The resulting increase in intracellular calcium causes fusion of vesicles with the surface membrane and exocytotic expulsion of acetylcholine and cotransmitters into the junctional cleft (see text). This step can he blocked by botulinum toxin. Acetylcholine s action is terminated by metabolism by the enzyme acetylcholinesterase. Receptors on the presynaptic nerve ending modulate transmitter release. SNAPs, synaptosome-associated proteins VAMPs, vesicle-associated membrane proteins.

As with pilocarpine and arecoline, increased interest in pharmacotherapy of Alzheimer s disease and other memory deficit conditions has led to renewed and expanded studies of oxotremorine. This compound has little or no effect on serum or red cell but3nyl-cholinesterase. Oxotremorine has been described as a potent muscarinic partial agonist (172). However, an earlier report (11) presented evidence that oxotremorine has an indirect action in the CNS, perhaps by stimulation of choline acetyltransferase, resulting in elevation of acetylcholine levels. The peripheral actions of oxotremorine, including effects on cardiovascular mechanisms, have been ascribed (172) to preferential activation of M, receptors. Brimblecomb (211, 212) reported... 

Acetylcholine (ACh) is synthesized from acetate and choline in the synaptic nave via choline acetyltransferase and is stored in the synaptic vesicles and released by Ca2 influx upon depolarization. The ACh then binds to a receptor on the other side of the synaptic junction, thereby transmitting the signal. Acetylcholinesterase (AChE) hydrolyzes the ACh and ends the signal. Cholinergic drugs are those that affect this process either by influencing ACh levels or by acting directly on the nicotinic or muscarinic receptors. 

Acetylcholine is synthesized from choline and acetyl coenzyme A through the action of the enzyme choline acetyltransferase and becomes packaged into membrane-bound vesicles. After the arrival of a nerve signal at the termination of an axon, the vesicles fuse with the cell membrane, causing the release of acetylcholine into the synaptic cleft. For the nerve signal to continue, acetylcholine must diffuse to another nearby neuron or muscle cell, where it will bind and activate a receptor protein. 

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