Nicotinic acetylcholine receptor, muscle-type (adult form) (nAChR (muscle, adult))

Nicotinic acetylcholine receptors (nAChRs) are pentameric ligand-gated ion channels that mediate excitatory neurotransmission in skeletal muscle and the nervous system in response to acetylcholine. The muscle-type nAChR is composed of five subunits: two α1, one β1, one δ, and either one γ subunit (fetal/embryonic type) or one ε subunit (adult type). The muscle nAChR is localized at the neuromuscular junction and plays an essential role in skeletal muscle contraction. It is the target of numerous therapeutic drugs (muscle relaxants), toxins (e.g., alpha-bungarotoxin), and autoantibodies (as in myasthenia gravis). The designation in the question, "alpha12beta gamma epsilon", is non-canonical and inconsistent with human gene/protein nomenclature; a twelfth alpha (alpha12) subunit is not recognized in mammalian systems[3][5][6]. Caveat: There is no "alpha12" nAChR subunit gene in mammals[3][5]. The canonical muscle nAChR alpha subunit is "alpha1" (gene symbol: CHRNA1). In embryos, the muscle nAChR is composed of α1, β1, δ, γ; after birth, γ is replaced by ε[6]. The provided name is therefore not an established target and should be standardized to the canonical muscle (adult) nicotinic acetylcholine receptor.

Other names

Muscle-type nicotinic acetylcholine receptorNMJ nAChRNicotinic acetylcholine receptor (α1)2β1δε (adult)Nicotinic acetylcholine receptor (α1)2β1δγ (fetal)

Agonists (activate channel and cause depolarization, leading to muscle contraction) Antagonists/Blockers (bind and prevent channel opening, leading to paralysis or muscle relaxation) Desensitizing agents (prolonged ligand exposure leads to longer-term inactivation)