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Novel Muscarinic Receptor Mutant Mouse Models

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Muscarinic Receptors

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 208))

Abstract

Muscarinic acetylcholine (ACh) receptors (mAChRs; M1–M5) regulate the activity of an extraordinarily large number of important physiological processes. During the past 10–15 years, studies with whole-body M1–M5 mAChR knockout mice have provided many new insights into the physiological and pathophysiological roles of the individual mAChR subtypes. This review will focus on the characterization of a novel generation of mAChR mutant mice, including mice in which distinct mAChR genes have been excised in a tissue- or cell type-specific fashion, various transgenic mouse lines that overexpress wild-type or different mutant M3 mAChRs in certain tissues or cells only, as well as a novel M3 mAChR knockin mouse strain deficient in agonist-induced M3 mAChR phosphorylation. Phenotypic analysis of these new animal models has greatly advanced our understanding of the physiological roles of the various mAChR subtypes and has identified potential targets for the treatment of type 2 diabetes, schizophrenia, Parkinson’s disease, drug addiction, cognitive disorders, and several other pathophysiological conditions.

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Abbreviations

ACh:

Acetylcholine

CNO:

Clozapine-N-oxide

DHPG:

((S)-3,5-dihydroxyphenylglycine

DREADD:

Designer receptor exclusively activated by designer drug

GH:

Growth hormone

GHRH:

Growth hormone-releasing hormone

GPCR:

G-protein-coupled receptor

i3 loop:

Third intracellular loop

IGF-1:

Insulin-like growth factor

KI:

Knockin

KO:

Knockout

LDP:

Long-term depression

LFP:

Local field potential

LTP:

Long-term potentiation

mAChR:

Muscarinic acetylcholine receptor

mGluR:

Metabotropic glutamate receptor

Oxo-M:

Oxotremorine M

PI:

Phosphatidylinositol

RASSL:

Receptor activated solely by synthetic ligand

SNS:

Sympathetic nervous system

T2D:

Type 2 diabetes

tTA:

tet Transactivator

WT:

Wild-type

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Acknowledgments

J. W. was supported by funding from the Intramural Research Program of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), NIH (Bethesda, MD, USA). I would like to thank all my present and past coworkers and collaborators for their invaluable contributions to the generation and phenotypical analysis of many of the new mAChR mutant mouse models reviewed in this chapter. I apologize to the many colleagues in the field whose work I was unable to cite due to space limitations.

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

    Jürgen Wess

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Correspondence to Jürgen Wess .

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Editors and Affiliations

  1. UHN67, Department of Pulmonary and Critical Ca, Oregon Health & Science University, SW Sam Jackson Park Road 3181, Portland, 97239, Oregon, USA

    Allison D. Fryer

  2. , Department of Pharmacology, Monash Institute of Pharmaceutical Scien, Royal Parade 381, Parkville, 3052, Victoria, Australia

    Arthur Christopoulos

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

    Neil M. Nathanson

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Wess, J. (2012). Novel Muscarinic Receptor Mutant Mouse Models. In: Fryer, A., Christopoulos, A., Nathanson, N. (eds) Muscarinic Receptors. Handbook of Experimental Pharmacology, vol 208. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-23274-9_6

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