Actions of acetylcholine in the periphery are the result of activation of either the ionotropic nicotinic receptor or the metabotropic muscarinic receptor. In the mammalian central nervous system (CNS) c, both nicotinic and muscarinic receptor subtypes are present on neurons, although there is as yet very limited evidence for a physiological role for nicotinic receptors in synaptic function in the mammalian brain (Role and Berg, 1996). In the periphery, among other effects, muscarinic receptors mediate smooth muscle contraction, glandular secretion, and modulation of cardiac rate and force. In the CNS, there is evidence that muscarinic receptors are involved in motor control, temperature regulation, cardiovascular regulation, and memory. Interest in the classification of muscarinic receptors involved in functions at different locations has been heightened by the potential therapeutic application of selective agents in areas such as Alzheimer’s disease, Parkinson’s disease, asthma, analgesia, and disorders of intestinal motility and cardiac and urinary bladder function. Historically, the first indications of the existence of muscarinic receptor subtypes were the cardioselective actions of gallamine (Riker and Wescoe, 1951) and the a Composition of the muscarinic receptor subcommittee of the International Union of Pharmacology Committee on Receptor Nomenclature and Drug Classification: NJM Birdsall (Chair), Division of Physical Biochemistry, National Institute for Medical Research, Mill Hill, London NW7 1AA, UK; NJ Buckley, Department of Pharmacology, Wellcome Laboratory of Molecular Pharmacology, University College London, Gower Street, London WC1E 6BT, UK; MP Caulfield, Department of Pharmacology, University of Dundee, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland; R. Hammer, Drug Discovery, Boehringer Ingelheim KG, Binger Straβe 173, D-55216 Ingelheim/Rhein, Germany; HJ Kilbinger, Pharmakologisches Institut, University of Mainz, Germany; G. Lambrecht, Department of Pharmacology, University of Frankfurt, Biocentre Niederursel, D-60439 Frankfurt, Germany; E. Mutschler, Department of Pharmacology, University of Frankfurt, Biocentre Niederursel, D-60439 Frankfurt, Germany; NM Nathanson, Department of Pharmacology, SJ-30, University of Washington, Seattle, WA 98195, USA; RD Schwarz, Parke-Davis Pharmacology Research Division, 2800 Plymouth Road, Ann Arbor, MI 48105, USA. b Address for correspondence: Nigel JM Birdsall, Division of Physical Biochemistry, National Institute for Medical Research, Mill Hill, London NW7 1AA, UK. E-mail: n. birdsa@ nimr. mrc. ac. uk. c Abbreviations: cAMP, cyclic adenosine monophosphate; CNS, central nervous system; LY297802,() 3-(S) 3-[4-butylthio-12, 5-thiadiazol-3-yl]-1-azabicyclo [2, 2, 2] octane; McN-A-343,(4-Hydroxy-2-butynyl) 1-trimethylammonium-m-chlorocarbanilate chloride; mRNA, messenger ribonucleic acid.