Nicotinic acetylcholine receptor alpha-3 subunit (CHRNA3)

The **nicotinic acetylcholine receptor alpha‑3 subunit** is a protein component encoded by the *CHRNA3* gene that assembles with other nicotinic receptor subunits—most commonly β4—to form functional pentameric ligand-gated ion channels known as neuronal nicotinic acetylcholine receptors. These receptors are predominantly expressed in autonomic ganglia and certain regions of the central nervous system where they mediate fast synaptic transmission via cation influx upon activation by endogenous acetylcholine or exogenous ligands like nicotine. The α3β4 subtype plays a critical role in regulating autonomic functions including cardiovascular responses and has been implicated genetically and pharmacologically in substance use disorders such as tobacco addiction. Drugs targeting this receptor can act either to stimulate its activity (as agonists) or inhibit it (as antagonists), making it an important therapeutic target for conditions ranging from hypertension to drug dependence.[1][2][4][7]

Other names

nAChR α3 subunitNeuronal acetylcholine receptor subunit alpha-3CHRNA3

Drugs targeting this molecule act primarily as **agonists** or **antagonists** at the ligand-binding site between subunits. Agonists activate the channel to allow cation influx (Na^+, K^+), leading to neuronal excitation. Antagonists block this action by preventing channel opening or modulating allosterically. Some drugs are partial agonists or noncompetitive antagonists that modulate activity without directly competing for the primary binding site[1][2].