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Neuronal acetylcholine receptor subunit beta-3 (CHRNB3) is a component of neuronal nicotinic acetylcholine receptors (nAChRs), which are pentameric ligand-gated ion channels mediating fast synaptic transmission in the central and peripheral nervous systems[1][5][6][7]. CHRNB3 is a beta-type subunit that participates in assembling functional nAChRs, particularly by co-assembling with other subunits such as CHRNA3, CHRNA4, CHRNA6, CHRNB2, and CHRNB4, influencing receptor properties like sensitivity to acetylcholine and nicotine, ion selectivity, and kinetics[1][6]. CHRNB3 has a mostly accessory role and can only form functional nAChRs when co-expressed with other nAChR beta subunits[1][6]. Genetic variation in CHRNB3 is strongly linked to risk for nicotine dependence and tobacco use disorder, likely by altering the rewarding and reinforcing effects of nicotine, and it may also play modulatory roles in other neuropsychiatric and movement disorders[3][1][5].
Agonists (e.g., nicotine, varenicline) bind and activate the receptor to facilitate cation (Na⁺, Ca²⁺) influx, leading to neuronal depolarization and neurotransmitter release Antagonists (e.g., mecamylamine) block receptor function, reducing neuronal excitation
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