Muscarinic acetylcholine receptor (M1–M5 subtypes) (mAChR (M1–M5))

The muscarinic acetylcholine receptors (M1–M5) are a family of G protein-coupled receptors (GPCRs) that mediate many physiological effects of acetylcholine in the central and peripheral nervous systems[3][5]. There are five well-characterized subtypes (M1, M2, M3, M4, M5), each with distinct tissue distributions and signaling properties: M1, M3, and M5 are primarily coupled to Gq proteins (stimulating the phospholipase C pathway and intracellular calcium mobilization), while M2 and M4 are coupled to Gi proteins (inhibiting adenylyl cyclase and lowering cAMP)[3]. Muscarinic receptors are broadly involved in cognitive function, autonomic control of heart and smooth muscle, and glandular secretions[3][9]. M1, M3, and M5 subtypes mediate excitatory effects such as vasodilation, smooth muscle contraction, and gland secretion, while M2 and M4 subtypes mediate inhibitory effects such as slowing heart rate and modulating neurotransmitter release[3]. The muscarinic receptor family has significant pharmacological relevance and is a therapeutic target in several conditions, including Alzheimer's disease, schizophrenia, bladder dysfunction, and cardiovascular disorders[5][6][7][8]. Selective targeting of muscarinic subtypes remains challenging due to conserved orthosteric binding sites, but subtype-selective ligands and allosteric modulators are under investigation[5][8]. **Note:** The input "M1–M5 muscarinic" refers to a group of related targets (the five subtypes of muscarinic acetylcholine receptor), not a single molecule. For structured data, each subtype (e.g., Muscarinic acetylcholine receptor M1) should be considered a separate canonical target. "M1–M5 muscarinic" is not a single canonical entity, so is_incorrect is set to true to reflect this[3][5][8].

Other names

muscarinic receptormuscarinic acetylcholine receptormAChRM1 receptorM2 receptorM3 receptorM4 receptorM5 receptor

Agonists mimic acetylcholine, stimulating muscarinic receptors to elicit physiological responses (e.g., smooth muscle contraction, glandular secretion)[3][4]. Antagonists block acetylcholine binding, inhibiting receptor-mediated effects (e.g., bronchodilation or reduction of gland secretion)[8]. Allosteric modulators alter receptor activity by binding non-orthosteric sites, potentially offering greater subtype selectivity[5][8].