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Muscarinic Acetylcholine Receptor Function
Published by Anonymous on 2007/9/30 (3558 reads)
1: Auton Autacoid Pharmacol. 2006 Jul;26(3):219-33.


Muscarinic receptor subtypes in neuronal and non-neuronal cholinergic function.

Eglen RM.

DiscoveRx Corp, 42501, Albrae St., Suite 100, Fremont, CA 94538, USA.

1 Muscarinic M1-M5 receptors mediate the metabotropic actions of acetylcholine in the nervous system. A growing body of data indicate they also mediate autocrine functions of the molecule. The availability of novel and selective muscarinic agonists and antagonists, as well as in vivo gene disruption techniques, has clarified the roles of muscarinic receptors in mediating both functions of acetylcholine. 2 Selective M1 agonists or mixed M1 agonists/M2 antagonists may provide an approach to the treatment of cognitive disorders, while M3 antagonism, or mixed M2/M3 antagonists, are approved for the treatment of contractility disorders including overactive bladder and chronic obstructive pulmonary disease. Preclinical data suggest that selective agonism of the M4 receptor will provide novel anti-nociceptive agents, while therapeutics-based upon agonism or antagonism of the muscarinic M5 receptor have yet to be reported. 3 The autocrine functions of muscarinic receptors broadly fall into two areas - control of cell growth or proliferation and mediation of the release of chemical mediators from epithelial cells, ultimately causing muscle relaxation. The former particularly are involved in embryological development, oncogenesis, keratinocyte function and immune responsiveness. The latter regulate contractility of smooth muscle in the vasculature, airways and urinary bladder. 4 Most attention has focused on muscarinic M1 or M3 receptors which mediate lymphocyte immunoresponsiveness, cell migration and release of smooth muscle relaxant factors. Muscarinic M4 receptors are implicated in the regulation of keratinocyte adhesion and M2 receptors in stem cell proliferation and development. Little data are available concerning the M5 receptor, partly due to the difficulties in defining the subtype pharmacologically. 5 The autocrine functions of acetylcholine, like those in the nervous system, involve activation of several muscarinic receptor subtypes. Consequently, the role of these subtypes in autocrine, as well neuronal cholinergic systems, significantly expands their importance in physiology and pathophysiology.

Publication Types:
Review

PMID: 16879488 [PubMed - indexed for MEDLINE]

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2: Cell Metab. 2006 Jun;3(6):390-2.


Comment on:
Cell Metab. 2006 Jun;3(6):449-61.

Ringing the dinner bell for insulin: muscarinic M3 receptor activity in the control of pancreatic beta cell function.

Gromada J, Hughes TE.

Diabetes and Metabolism Disease Area, Novartis Institutes for BioMedical Research, 100 Technology Square, Cambridge, Massachusetts 02139, USA.

In this issue of Cell Metabolism, Gautam et al. (2006) show that pancreatic beta cell M3 muscarinic acetylcholine receptors control insulin secretion. Their results highlight the role of the M3 receptor subtype in integrating nervous stimuli with metabolic control of insulin secretion and glucose homeostasis.

Publication Types:
Comment
Review

PMID: 16753574 [PubMed - indexed for MEDLINE]

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3: Life Sci. 2003 Dec 5;74(2-3):345-53.


Novel insights into M5 muscarinic acetylcholine receptor function by the use of gene targeting technology.

Yamada M, Basile AS, Fedorova I, Zhang W, Duttaroy A, Cui Y, Lamping KG, Faraci FM, Deng CX, Wess J.

Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bldg. 8A, Room B1A-05, 8 Center Drive MSC 0810, Bethesda, MD 20892-0810, USA.

Until recently, little was known about the possible physiological functions of the M(5) muscarinic acetylcholine receptor subtype, the last member of the muscarinic receptor family (M(1)-M(5)) to be cloned. To learn more about the potential physiological roles of this receptor subtype, we generated and analyzed M(5) receptor-deficient mice (M5 -/- mice). Strikingly, acetylcholine, a potent dilator of most vascular beds, virtually lost the ability to dilate cerebral arteries and arterioles in M5 -/- mice, suggesting that endothelial M(5) receptors mediate this activity in wild-type mice. This effect was specific for cerebral blood vessels, since acetylcholine-mediated dilation of extra-cerebral arteries remained fully intact in M5 -/- mice. In addition, in vitro neurotransmitter release experiments indicated that M(5) receptors located on dopaminergic nerve terminals play a role in facilitating muscarinic agonist-induced dopamine release in the striatum, consistent with the observation that the dopaminergic neurons innervating the striatum almost exclusively express the M(5) receptor subtype. We also found that the rewarding effects of morphine, the prototypical opiate analgesic, were substantially reduced in M5 -/- mice, as measured in the conditioned place preference paradigm. Furthermore, both the somatic and affective components of naloxone-induced morphine withdrawal symptoms were significantly attenuated in M5 -/- mice. It is likely that these behavioral deficits are caused by the lack of mesolimbic M(5) receptors, activation of which is known to stimulate dopamine release in the nucleus accumbens. These results convincingly demonstrate that the M(5) muscarinic receptor is involved in modulating several important pharmacological and behavioral functions. These findings may lead to novel therapeutic strategies for the treatment of drug addiction and certain cerebrovascular disorders.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 14607263 [PubMed - indexed for MEDLINE]

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4: Trends Pharmacol Sci. 2003 Aug;24(8):414-20.


Novel insights into muscarinic acetylcholine receptor function using gene targeting technology.

Wess J.

Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Department of Health and Human Services, Bethesda, MD 20892, USA. jwess@helix.nih.gov

Muscarinic acetylcholine receptors (mAChRs) modulate the activity of an extraordinarily large number of physiological functions. Individual members of the mAChR family (M(1)-M(5)) are expressed in a complex, overlapping fashion in most tissues and cell types. However, the identification of the precise physiological roles of individual mAChR subtypes remains a challenging task because, with the exception of a few snake toxins, mAChR ligands that can activate or inhibit specific mAChR subtypes with a high degree of selectivity are not yet available. Knowledge of the specific roles of mAChR subtypes is of considerable interest for the development of novel, clinically useful mAChR ligands. In this article, recent studies of mutant mouse strains developed, using gene targeting techniques, to be deficient in one of the three G(q)-coupled mAChR subtypes (M(1), M(3) and M(5)) are discussed. These investigations have led to many important new insights into the physiological roles of these receptor subtypes.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 12915051 [PubMed - indexed for MEDLINE]

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5: Basic Res Cardiol. 2001 Nov;96(6):528-38.


Presence, distribution and physiological function of adrenergic and muscarinic receptor subtypes in the human heart.

Brodde OE, Bruck H, Leineweber K, Seyfarth T.

Institute of Pharmacology and Toxicology, Martin-Luther-University of Halle-Wittenberg, Halle/Saale, Germany. otto-erich.brodde@medizin.uni-halle.de

The sympathetic and parasympathetic nervous system play a powerful role in controlling cardiac function by activating adrenergic and muscarinic receptors. In the human heart there exist alpha1-, beta1- and beta2-adrenoceptors and M2-muscarinic receptors and possibly also (prejunctional) alpha2-adrenoceptors. Beta1- and beta2-adrenoceptors are quite evenly distributed in the human heart while M2-receptors are heterogeneously distributed (more receptors in atria than in ventricles). Stimulation of beta1- and beta2-adrenoceptors causes increases in heart rate and force of contraction while stimulation of M2-receptors decreases heart rate (directly in atria) and force of contraction (indirectly in ventricles). Pathological situations (such as heart failure) or pharmacological interventions (for example, beta-blocker treatment) can alter the distribution of beta1- and beta2-adrenoceptors in the human heart, while M2-receptors are only marginally affected. On the other hand, relatively little is known on distribution and functional role of alpha1- and alpha2-adrenoceptor subtypes in the human heart.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 11770070 [PubMed - indexed for MEDLINE]

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6: Ann N Y Acad Sci. 2000;915:237-46.


Stress-induced decrease of the intestinal barrier function. The role of muscarinic receptor activation.

Groot J, Bijlsma P, Van Kalkeren A, Kiliaan A, Saunders P, Perdue M.

Institute for Neurobiology, University of Amsterdam, Amsterdam, The Netherlands. groot@bio.uva.nl

Recently the breakdown of the barrier function of the intestinal epithelium after application of an experimental psychological and physical stress protocol in rats has been observed. Not only did smaller molecules pass from the luminal to the serosal side, but so also did larger proteins with the dimensions of luminal antigens and toxins. The increased permeability for macromolecules is primarily due to a decrease of the tightness of the zonula occludens, but an increased endocytotic uptake indicates that transcytosis is increased also. From studies of model systems it can be concluded that activation of the intracellular protein kinase C route by muscarinic receptor activation or histamine receptor activation can be one of the underlying cellular pathways. The physical pathway relaying the stress from the brain to the intestinal tract appears to be the parasympathetic branch of the autonomic nervous system. The difference in reaction of different strains suggests that coping style is an important determinant of the response of the intestinal barrier to stress.

Publication Types:
Review

PMID: 11193581 [PubMed - indexed for MEDLINE]

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7: Life Sci. 1999;64(6-7):449-55.


Effects of inflammatory cells on neuronal M2 muscarinic receptor function in the lung.

Fryer AD, Adamko DJ, Yost BL, Jacoby DB.

Department of Physiology, Johns Hopkins School of Public Health and Hygiene, Baltimore, MD, USA.

In the lungs, acetylcholine released from the parasympathetic nerves stimulates M3 muscarinic receptors on airway smooth muscle inducing contraction and bronchoconstriction. The amount of acetylcholine released from these nerves is limited locally by neuronal M2 muscarinic receptors. These neuronal receptors are dysfunctional in asthma and in animal models of asthma. Decreased M2 muscarinic receptor function results in increased release of acetylcholine and in airway hyperreactivity. Inflammation has long been associated with hyperreactivity and the role of inflammatory cells in loss of neuronal M2 receptor function has been examined. There are several different mechanisms for loss of neuronal M2 receptor function. These include blockade by endogenous antagonists such as eosinophil major basic protein, decreased expression of M2 receptors following infection with viruses or exposure to pro inflammatory cytokines such as gamma interferon. Finally, the affinity of acetylcholine for these receptors can be decreased by exposure to neuraminidase.

Publication Types:
Review

PMID: 10069509 [PubMed - indexed for MEDLINE]

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8: Life Sci. 1999;64(6-7):375-9.


Molecular analysis of the regulation of muscarinic receptor expression and function.

Nadler LS, Rosoff ML, Hamilton SE, Kalaydjian AE, McKinnon LA, Nathanson NM.

Department of Pharmacology, University of Washington, Seattle 98195-7750, USA.

We have investigated the molecular mechanisms involved in the regulation of muscarinic acetylcholine receptor gene expression and localization and generated knockout mice to study the role of the M1 muscarinic receptor in vivo. We have used the MDCK cell system to demonstrate that different subtypes of mAChR can be targeted to different regions of polarized cells. We have also examined the developmental regulation of mAChR expression in the chick retina. Early in development, the M4 receptor is the predominant mAChR while the levels of the M2 and M3 receptors increase later in development. The level of M2 receptor is also initially very low in retinal cultures and undergoes a dramatic increase over several days in vitro. The level of M2 receptor can be increased by a potentially novel, developmentally regulated, secreted factor produced by retinal cells. The promoter for the chick M2 receptor gene has been isolated and shown to contain a site for GATA-family transcription factors which is required for high level cardiac expression. The M2 promoter also contains sites which mediate induction of transcription in neural cells by neurally active cytokines. We have generated knockout mice lacking the M1 receptor and shown that these mice do not exhibit pilocarpine-induced seizures and muscarinic agonist-induced suppression of the M-current potassium channel in sympathetic neurons.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 10069499 [PubMed - indexed for MEDLINE]

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9: Thorax. 1998 Jul;53(7):613-6.


Pulmonary neuronal M2 muscarinic receptor function in asthma and animal models of hyperreactivity.

Costello RW, Jacoby DB, Fryer AD.

Department of Medicine, University of Liverpool, UK.

In the lungs neuronal M2 muscarinic receptors limit acetylcholine release from postganglionic cholinergic nerves. These inhibitory M2 receptors are dysfunctional in antigen challenged guinea pigs and in humans with asthma which leads to an increase in vagally mediated hyperreactivity. In vitro, eosinophil products act as allosteric antagonists at neuronal M2 muscarinic receptors. In vivo, displacing or neutralising MBP preserves neuronal M2 muscarinic receptor function and prevents hyperreactivity. Thus, there is good evidence from animal studies that after antigen challenge pulmonary M2 muscarinic receptors become dysfunctional because MBP inhibits their function. Loss of function of pulmonary neuronal M2 muscarinic receptors has also been reported in patients with asthma, although the clinical significance of this dysfunction and the mechanisms underlying it are not yet established.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 9797763 [PubMed - indexed for MEDLINE]

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10: Trends Pharmacol Sci. 1998 Aug;19(8):322-7.


Regulation of the expression and function of the M2 muscarinic receptor.

Haddad el-B , Rousell J.

Department of Pharmacology, Rhône-Poulenc Rorer, Dagenharn, UK.

Since the cloning and expression of many of the G protein-coupled receptors during the 1980s, there has been a massive increase in our understanding of many aspects of their function. The use of molecular biology to engineer and express mutant receptors has made it possible to determine key amino acids involved in receptor function. Although advances in molecular biology have contributed greatly to our understanding of the pharmacology and structure of the five subtypes of muscarinic receptor, much remains to be learned about the factors that regulate their expression and function. This review by El-Bdaoui Haddad and Jonathan Rousell describes the current state of awareness and highlights recent advances made in the elucidation of the mechanisms involved in muscarinic receptor regulation. Because most is known about the regulation of expression of the M2 receptor subtype, particular attention will be paid to it. Furthermore, this receptor subtype plays an important role in regulating acetylcholine output from airway cholinergic nerves, and there is substantial evidence from studies both in vivo and in vitro in human and animal models that these receptors are dysfunctional in asthma.

Publication Types:
Research Support, Non-U.S. Gov't
Review

PMID: 9745360 [PubMed - indexed for MEDLINE]

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11: Life Sci. 1997;60(13-14):1101-4.


Regulation of muscarinic receptor expression and function in cultured cells and in knock-out mice.

McKinnon LA, Rosoff M, Hamilton SE, Schlador ML, Thomas SL, Nathanson NM.

Department of Pharmacology, University of Washington, Seattle 98195-7750, USA.

We have investigated the molecular and cellular basis for the regulation of expression and function of the muscarinic acetylcholine receptors. Treatment of cultured chick cardiac cells with the agonist carbachol results in decreased levels of mRNA encoding the m2 and m4 receptors. Treatment of chick embryos in ovo with carbachol results in decreased levels of mRNA encoding the potassium channel subunits GIRK1 and GIRK4 as well as the m2 receptor. There are thus multiple pathways for the regulation of mAChR responsiveness by long-term agonist exposure. Immunoblot, immunoprecipitation, and solution hybridization analyses have been used to quantitate the regulation of mAChR expression in chick retina during embryonic development. The m4 receptor is the predominant subtype expressed early in development, while the expression of the m3 and m2 receptors increases later in development. A cAMP-regulated luciferase reporter gene has been used to demonstrate that the m2 and m4 receptors have distinct specificities for coupling to G-protein subtypes to mediate inhibition of adenylyl cyclase. This system has also been used to demonstrate that beta-arrestin1 and beta-adrenergic receptor kinase-1 act synergistically to promote receptor desensitization. We have isolated the promoter region for the chick m2 receptor gene, identified regions of the promoter required to drive high level expression in cardiac and neural cells, and have identified a region which confers sensitivity of gene expression to neurally active cytokines. Finally, in order to determine the role of individual receptor subtypes in muscarinic-mediated responses in vivo, we have used the method of targeted gene disruption by homologous recombination to generate mice deficient in the m1 receptor.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 9121353 [PubMed - indexed for MEDLINE]

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12: Pharmacol Rev. 1996 Dec;48(4):531-65.


Muscarinic receptor subtypes and smooth muscle function.

Eglen RM, Hegde SS, Watson N.

Institute of Pharmacology, Roche Bioscience, Palo Alto, California 94304, USA.

Publication Types:
Review

PMID: 8981565 [PubMed - indexed for MEDLINE]

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13: Prog Brain Res. 1996;109:165-8.


Regulation of muscarinic acetylcholine receptor expression and function.

Nathanson NM.

Department of Pharmacology, University of Washington, Seattle 98195-7750, USA.

Publication Types:
Review

PMID: 9009703 [PubMed - indexed for MEDLINE]

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14: Prog Brain Res. 1996;109:153-62.


Molecular aspects of muscarinic receptor assembly and function.

Wess J, Blin N, Yun J, Schöneberg T, Liu J.

Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, USA.

Publication Types:
Review

PMID: 9009702 [PubMed - indexed for MEDLINE]

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15: Proc West Pharmacol Soc. 1996;39:57-60.


Muscarinic M2 and M3 receptor function in smooth muscle.

Eglen RM.

Institute of Pharmacology, Roche Bioscience, Palo Alto, CA 94304, USA.

Publication Types:
Review

PMID: 8895970 [PubMed - indexed for MEDLINE]

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16: Life Sci. 1995;56(11-12):939-43.


Molecular analysis of the regulation of muscarinic receptor expression and function.

Hamilton SE, McKinnon LA, Jackson DA, Goldman PS, Migeon JC, Habecker BA, Thomas SL, Nathanson NM.

Department of Pharmacology, University of Washington, Seattle 98195, USA.

Several systems are being used to determine the molecular and cellular basis for the regulation of expression and function of the muscarinic receptors. Treatment of chick heart cells in culture results in decreased levels of mRNA encoding the cm2 and cm4 receptors. This probably results from decreased gene transcription which requires concomitant mAChR-mediated inhibition of adenylyl cyclase and mAChR-mediated stimulation of phospholipase C. Site-directed mutagenesis was used to demonstrate that the single tyrosine residue in the carboxyl-terminal cytoplasmic tail of the m2 receptor is involved in agonist-induced down-regulation but not sequestration. Activation of heterologous receptors in chick heart cells can also regulate mAChR mRNA levels. A cAMP-regulated luciferase reporter gene, has been used to demonstrate that the m4 receptor preferentially couples to Gi alpha-2 or Go alpha over Gi alpha-1 or Gi alpha-3 to mediate inhibition of adenylyl cyclase activity. Finally, in order to determine the role of individual receptor subtypes in muscarinic-mediated responses in vivo, we are beginning to use the method of targeted gene disruption by homologous recombination to generate mice deficient in specific receptor subtypes.

Publication Types:
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 10188796 [PubMed - indexed for MEDLINE]

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17: Trends Pharmacol Sci. 1993 Aug;14(8):308-13.


Molecular basis of muscarinic acetylcholine receptor function.

Wess J.

National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Laboratory of Bio-organic Chemistry, Bethesda, MD 20892.

Muscarinic acetylcholine receptors play important roles in numerous physiological functions including higher cognitive processes such as memory and learning. Consistent with the well-documented pharmacological heterogeneity of muscarinic receptors, molecular cloning studies have revealed the existence of five distinct muscarinic receptor proteins (M1-M5). Structure-function relationship studies of the cloned receptors have been greatly aided by the high degree of structural homology that muscarinic receptors share with other G protein-coupled receptors. In this review, Jürgen Wess discusses recent mutagenesis studies that have considerably advanced our knowledge of the molecular details underlying muscarinic receptor function.

Publication Types:
Review

PMID: 8249149 [PubMed - indexed for MEDLINE]

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18: Prog Brain Res. 1993;98:121-7.


Muscarinic acetylcholine receptor subtypes: localization and structure/function.

Brann MR, Ellis J, Jørgensen H, Hill-Eubanks D, Jones SV.

Department of Psychiatry, University of Vermont, Burlington 05405.

Based on the sequence of the five cloned muscarinic receptor subtypes (m1-m5), subtype selective antibody and cDNA probes have been prepared. Use of these probes has demonstrated that each of the five subtypes has a markedly distinct distribution within the brain and among peripheral tissues. The distributions of these subtypes and their potential physiological roles are discussed. By use of molecular genetic manipulation of cloned muscarinic receptor cDNAs, the regions of muscarinic receptors that specify G-protein coupling and ligand binding have been defined in several recent studies. Overall, these studies have shown that amino acids within the third cytoplasmic loop of the receptors define their selectivities for different G-proteins and that multiple discontinuous epitopes contribute to their selectivities for different ligands. The residues that contribute to ligand binding and G-protein coupling are described, as well as the implied structures of these functional domains.

Publication Types:
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 8248499 [PubMed - indexed for MEDLINE]

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19: Trends Pharmacol Sci. 1989 Dec;Suppl:43-6.


Regulation of muscarinic acetylcholine receptor function in cardiac cells and in cells expressing cloned receptor genes.

Shapiro RA, Tietje KM, Subers EM, Scherer NM, Habecker BA, Nathanson NM.

The regulation of the number and function of the muscarinic receptors has been investigated in cultured chick cardiac cells and in cells expressing cloned genes encoding mammalian, Drosophila, and chick muscarinic receptors. A serum-free defined medium for the culture of chick embryonic heart cells has been used to study the regulation of mAChR number and function by serum lipoproteins. Addition of rooster high density lipoprotein to the culture medium results in an attenuation of muscarinic receptor-mediated inhibition of cAMP accumulation without a change in the number of receptors or inhibitory G proteins. Clones encoding the mouse m1 receptor and a homologous receptor from Drosophila have been isolated. When expressed in Y1 adrenal cells, both receptors stimulate phosphoinositide hydrolysis but do not inhibit cAMP accumulation. Deletion of 123 out of the 156 amino acids in the third cytoplasmic loop of the mouse m1 receptor does not impair its ability to stimulate phosphoinositide hydrolysis. A genomic clone encoding a muscarinic receptor expressed in chick heart has been isolated. When expressed in Y1 cells, it causes inhibition of cAMP accumulation but does not stimulate phosphoinositide hydrolysis.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 2694522 [PubMed - indexed for MEDLINE]

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20: Trends Pharmacol Sci. 1988 Feb;Suppl:25-8.


Biochemical and immunological studies on the regulation of cardiac and neuronal muscarinic acetylcholine receptor number and function.

Subers EM, Liles WC, Luetje CW, Nathanson NM.

Publication Types:
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.
Review

PMID: 3074532 [PubMed - indexed for MEDLINE]
 

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