Nicotinic acetylcholine receptors (nAChRs) mediate the physiological effects of exogenous nicotine. They also play critical physiological roles throughout the brain and body by mediating cholinergic excitatory neurotransmission, modulating the release of neurotransmitters, and have longer-term effects on gene expression and cellular connections¹.

nAChRs are pentameric complexes made up of combinations of a number of different nAChR subunits, which can be classified as α subunits, containing two cysteine residues at positions analogous to Cys192 and Cys193, and non-alpha subunits (‘structural’ subunits), which can be defined as β subunits when they are expressed in the vertebrate nervous system².  There are nine α subunits (α2–α10) and three β subunits (β2, β3, and β4) in the CNS³. Nicotinic receptors are assembled as combinations of α (2-6) and and β (2-4) subunits. 

All α subunits are expressed in neuronal cells except for the α1 subunit which is specifically expressed in skeletal muscle. They are also expressed in non-neuronal cells such as bronchial epithelial cells⁴, as well lymphocytes⁵.

In humans, a mutant α2 subunit has been identified, which forms nAChRs with increased agonist sensitivity and causes a form of familial epilepsy⁶. Further, an α2 subunit null mouse model has been used to demonstrate a role for α2 nAChR in nicotine-induced modulation of long-term potentiation in the mouse hippocampal CA1 region, which may underlie some of the cognitive effects of nicotine⁷.