Neuronal acetylcholine receptor subunit alpha-3 and Neuronal acetylcholine receptor subunit beta-4 (nAChR α3β4)

The **neuronal acetylcholine receptor subunits alpha-3 and beta-4** form the heteropentameric **α3β4 nicotinic acetylcholine receptor**, a ligand-gated ion channel highly enriched in **autonomic ganglia** and the **adrenal medulla**. Activation by acetylcholine or exogenous agonists opens a transmembrane pore, allowing rapid cation (Na^+, K^+, and some Ca^2+^) influx, mediating fast excitatory synaptic transmission in the peripheral and select central circuits. This receptor modulates autonomic function and participates in neural circuits related to reward and addiction. α3β4-selective antagonists and modulators are being investigated as therapeutics for substance use disorders, though off-target effects due to the wide distribution of autonomic neurons present challenges for clinical applications[2][4][6][8].

Other names

Alpha-3 beta-4 nicotinic receptorα3β4 nicotinic acetylcholine receptorGanglion-type nicotinic receptorCHRNA3/CHRNB4 receptor

Agonists bind to the extracellular domain at the α3/β4 interface, inducing a conformational change that opens the ion channel, permitting cation influx and neuronal depolarization[1][4]. Antagonists block the agonist-binding site or the ion pore, inhibiting channel opening and reducing neuronal excitability or synaptic transmission[2][4].