Muscarinic acetylcholine receptor M3

From Wikipedia the free encyclopedia

CHRM3
Available structures
PDBOrtholog search: PDBe RCSB
Identifiers
AliasesCHRM3, EGBRS, HM3, PBS, cholinergic receptor muscarinic 3
External IDsOMIM: 118494; MGI: 88398; HomoloGene: 20191; GeneCards: CHRM3; OMA:CHRM3 - orthologs
Orthologs
SpeciesHumanMouse
Entrez
Ensembl
UniProt
RefSeq (mRNA)

NM_033269

RefSeq (protein)

NP_150372

Location (UCSC)Chr 1: 239.39 – 239.92 MbChr 13: 9.93 – 10.41 Mb
PubMed search[3][4]
Wikidata
View/Edit HumanView/Edit Mouse

The muscarinic acetylcholine receptor, also known as cholinergic/acetylcholine receptor M3, or the muscarinic 3, is a muscarinic acetylcholine receptor encoded by the human gene CHRM3.[5]

The M3 muscarinic receptors are located at many places in the body, e.g., smooth muscles, the bladder, the endocrine glands, the exocrine glands, lungs, pancreas and the brain. In the CNS, they induce emesis. Muscarinic M3 receptors are expressed in regions of the brain that regulate insulin homeostasis, such as the hypothalamus and dorsal vagal complex of the brainstem.[6] These receptors are highly expressed on pancreatic beta cells and are critical regulators of glucose homoestasis by modulating insulin secretion.[7] In general, they cause smooth muscle contraction and increased glandular secretions.[5]

They are unresponsive to PTX and CTX.

Mechanism

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Like the M1 muscarinic receptor, M3 receptors are coupled to G proteins of class Gq, which upregulate phospholipase C and, therefore, inositol trisphosphate and intracellular calcium as a signalling pathway.[8] The calcium function in vertebrates also involves activation of protein kinase C and its effects.

Effects

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Smooth muscle

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Because the M3 receptor is Gq-coupled and mediates an increase in intracellular calcium, it typically causes constriction of smooth muscle, such as that observed during bronchoconstriction. However, with respect to vasculature, activation of M3 on vascular endothelial cells causes increased synthesis of nitric oxide, which diffuses to adjacent vascular smooth muscle cells and causes their relaxation and vasodilation, thereby explaining the paradoxical effect of parasympathomimetics on vascular tone and bronchiolar tone. Indeed, direct stimulation of vascular smooth muscle M3 mediates vasoconstriction in pathologies wherein the vascular endothelium is disrupted.[9]

Diabetes

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The muscarinic M3 receptor regulates insulin secretion from the pancreas[7] and are an important target for understanding the mechanisms of type 2 diabetes mellitus.

Some antipsychotic drugs that are prescribed to treat schizophrenia and bipolar disorder (such as olanzapine and clozapine) have a high risk of diabetes side-effects. These drugs potently bind to and block the muscarinic M3 receptor, which causes insulin dysregulation that may precede diabetes.[6]

Other

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The M3 receptors are also located in many glands, both endocrine and exocrine glands, and help to stimulate secretion in salivary glands and other glands of the body.

Other effects are:

Ligands

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Agonists

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No highly selective M3 agonists are yet available as of 2018, but a number of non-selective muscarinic agonists are active at M3.

Antagonists

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Interactions

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Muscarinic acetylcholine receptor M3 has been shown to pre-couple with Gq proteins. The polybasic c-tail of the receptor is necessary for the pre-coupling.[8] It has also been shown to interact with Arf6[13] and ARF1.[13]

See also

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References

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  1. ^ a b c GRCh38: Ensembl release 89: ENSG00000133019Ensembl, May 2017
  2. ^ a b c GRCm38: Ensembl release 89: ENSMUSG00000046159Ensembl, May 2017
  3. ^ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  4. ^ "Mouse PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  5. ^ a b "Entrez Gene: CHRM3 cholinergic receptor, muscarinic 3".
  6. ^ a b Weston-Green K, Huang XF, Lian J, Deng C (May 2012). "Effects of olanzapine on muscarinic M3 receptor binding density in the brain relates to weight gain, plasma insulin and metabolic hormone levels". European Neuropsychopharmacology. 22 (5): 364–373. doi:10.1016/j.euroneuro.2011.09.003. PMID 21982116. S2CID 31739607.
  7. ^ a b Gautam D, Han SJ, Hamdan FF, Jeon J, Li B, Li JH, et al. (June 2006). "A critical role for beta cell M3 muscarinic acetylcholine receptors in regulating insulin release and blood glucose homeostasis in vivo". Cell Metabolism. 3 (6): 449–461. doi:10.1016/j.cmet.2006.04.009. hdl:10533/177761. PMID 16753580.
  8. ^ a b c Qin K, Dong C, Wu G, Lambert NA (August 2011). "Inactive-state preassembly of G(q)-coupled receptors and G(q) heterotrimers". Nature Chemical Biology. 7 (10): 740–747. doi:10.1038/nchembio.642. PMC 3177959. PMID 21873996.
  9. ^ Keith Parker, Laurence Brunton, Goodman, Louis Sanford, Lazo, John S., Gilman, Alfred (2006). Goodman & Gilman's the pharmacological basis of therapeutics (11th ed.). New York: McGraw-Hill. pp. 185. ISBN 0-07-142280-3.
  10. ^ a b c d e f Rang HP, Dale MM, Ritter JM, Moore PK (2003). "Ch. 10". Pharmacology (5th ed.). Elsevier Churchill Livingstone. pp. 139. ISBN 0-443-07145-4.
  11. ^ Shiga Y, Minami K, Shiraishi M, Uezono Y, Murasaki O, Kaibara M, Shigematsu A (November 2002). "The inhibitory effects of tramadol on muscarinic receptor-induced responses in Xenopus oocytes expressing cloned M(3) receptors". Anesthesia and Analgesia. 95 (5): 1269–73, table of contents. doi:10.1097/00000539-200211000-00031. PMID 12401609. S2CID 39621215.
  12. ^ Edwards Pharmaceuticals, Inc., Belcher Pharmaceuticals, Inc. (May 2010). "DailyMed". U.S. National Library of Medicine. Retrieved January 13, 2013.
  13. ^ a b Mitchell R, Robertson DN, Holland PJ, Collins D, Lutz EM, Johnson MS (September 2003). "ADP-ribosylation factor-dependent phospholipase D activation by the M3 muscarinic receptor". The Journal of Biological Chemistry. 278 (36): 33818–33830. doi:10.1074/jbc.M305825200. PMID 12799371.

Further reading

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This article incorporates text from the United States National Library of Medicine, which is in the public domain.