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The correct title of this article is Muscarinic acetylcholine receptor M3. It appears incorrectly here because of technical restrictions.

Cholinergic receptor, muscarinic 3
Symbol(s) CHRM3; HM3
External IDs OMIM: 118494 MGI88398 Homologene20191
Human Mouse Entrez 1131 12671 Ensembl na ENSMUSG00000046159 Uniprot na Q542R4 Refseq XM_001130695 (mRNA)
XP_001130695 (protein)
NM_033269 (mRNA)
NP_150372 (protein)
Location na Chr 13: 9.88 - 9.88 Mb
Pubmed search [1] [2]

The muscarinic acetylcholine receptor M3, also known as the cholinergic receptor, muscarinic 3, is a muscarinic acetylcholine receptor. It is encoded by the human gene CHRM3.[1]

The M3 muscarinic receptors are located at many places in the body, e.g. smooth muscles, endocrine, in exocrine glands, as well as in the lungs. They are also found in the CNS, where it induces emesis They generally cause smooth muscle contraction and increased glandular secretions.[1]

They are unresponsive to PTX and CTX.

Mechanism[edit | edit source]

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

Effects[edit | edit source]

Smooth muscle[edit | edit source]

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 whereby the vascular endothelium is disrupted.[2]

Other[edit | edit source]

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:

Agonists[edit | edit source]

Antagonists[edit | edit source]

See also[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 Entrez Gene: CHRM3 cholinergic receptor, muscarinic 3.
  2. Keith Parker; Laurence Brunton; Goodman, Louis Sanford; Lazo, John S.; Gilman, Alfred (2006). Goodman & Gilman's the pharmacological basis of therapeutics, 11th Ed., page 185, New York: McGraw-Hill.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 Rang HP, Dale MM, Ritter JM, Moore PK (2003). "Ch. 10" Pharmacology, 5th edition, page 139, Elsevier Churchill Livingstone. ISBN 0-443-07145-4.

Further reading[edit | edit source]

  • Goyal RK (1989). Muscarinic receptor subtypes. Physiology and clinical implications.. N. Engl. J. Med. 321 (15): 1022-9.
  • Eglen RM, Reddy H, Watson N, Challiss RA (1994). Muscarinic acetylcholine receptor subtypes in smooth muscle.. Trends Pharmacol. Sci. 15 (4): 114-9.
  • Brann MR, Ellis J, Jørgensen H, et al. (1994). Muscarinic acetylcholine receptor subtypes: localization and structure/function.. Prog. Brain Res. 98: 121-7.
  • Gutkind JS, Novotny EA, Brann MR, Robbins KC (1991). Muscarinic acetylcholine receptor subtypes as agonist-dependent oncogenes.. Proc. Natl. Acad. Sci. U.S.A. 88 (11): 4703-7.
  • Ashkenazi A, Ramachandran J, Capon DJ (1989). Acetylcholine analogue stimulates DNA synthesis in brain-derived cells via specific muscarinic receptor subtypes.. Nature 340 (6229): 146-50.
  • Bonner TI, Buckley NJ, Young AC, Brann MR (1987). Identification of a family of muscarinic acetylcholine receptor genes.. Science 237 (4814): 527-32.
  • Bonner TI, Young AC, Brann MR, Buckley NJ (1990). Cloning and expression of the human and rat m5 muscarinic acetylcholine receptor genes.. Neuron 1 (5): 403-10.
  • Peralta EG, Ashkenazi A, Winslow JW, et al. (1988). Distinct primary structures, ligand-binding properties and tissue-specific expression of four human muscarinic acetylcholine receptors.. EMBO J. 6 (13): 3923-9.
  • Blin N, Yun J, Wess J (1995). Mapping of single amino acid residues required for selective activation of Gq/11 by the m3 muscarinic acetylcholine receptor.. J. Biol. Chem. 270 (30): 17741-8.
  • Crespo P, Xu N, Daniotti JL, et al. (1994). Signaling through transforming G protein-coupled receptors in NIH 3T3 cells involves c-Raf activation. Evidence for a protein kinase C-independent pathway.. J. Biol. Chem. 269 (33): 21103-9.
  • Haga K, Kameyama K, Haga T, et al. (1996). Phosphorylation of human m1 muscarinic acetylcholine receptors by G protein-coupled receptor kinase 2 and protein kinase C.. J. Biol. Chem. 271 (5): 2776-82.
  • Szekeres PG, Koenig JA, Edwardson JM (1998). The relationship between agonist intrinsic activity and the rate of endocytosis of muscarinic receptors in a human neuroblastoma cell line.. Mol. Pharmacol. 53 (4): 759-65.
  • von der Kammer H, Mayhaus M, Albrecht C, et al. (1998). Muscarinic acetylcholine receptors activate expression of the EGR gene family of transcription factors.. J. Biol. Chem. 273 (23): 14538-44.
  • Ndoye A, Buchli R, Greenberg B, et al. (1998). Identification and mapping of keratinocyte muscarinic acetylcholine receptor subtypes in human epidermis.. J. Invest. Dermatol. 111 (3): 410-6.
  • Goodchild RE, Court JA, Hobson I, et al. (1999). Distribution of histamine H3-receptor binding in the normal human basal ganglia: comparison with Huntington's and Parkinson's disease cases.. Eur. J. Neurosci. 11 (2): 449-56.
  • Sato KZ, Fujii T, Watanabe Y, et al. (1999). Diversity of mRNA expression for muscarinic acetylcholine receptor subtypes and neuronal nicotinic acetylcholine receptor subunits in human mononuclear leukocytes and leukemic cell lines.. Neurosci. Lett. 266 (1): 17-20.
  • Budd DC, McDonald JE, Tobin AB (2000). Phosphorylation and regulation of a Gq/11-coupled receptor by casein kinase 1alpha.. J. Biol. Chem. 275 (26): 19667-75.

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


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