Nicotine, as the primary psychoactive component of tobacco smoke, binds to neuronal nicotinic acetylcholine receptors (nAChRs), a family of ligand-gated ion channels [7], facilitating various neurotransmitter release such as dopamine, glutamate, serotonin and γ-aminobutyric acid (GABA) [8–10] and thereby producing a number of neurophysiological and behavioral effects. Emerging evidence suggests that repeated exposure to nicotine can alter the level or types of genes expressed in multiple brain regions and such alteration ultimately mediates the functions of the related neurons and neural circuits. Numerous studies aiming to discover genetic variants or candidate genes, such as genome-wide association studies, genome-wide linkage scan, gene expression and candidate gene association studies, have found a large number of promising genes and chromosomal regions involved in the etiology of nicotine addiction [11–13]. Moreover, various neural pathways and transmitter systems have emerged as compelling candidates for the processing of addictive properties of nicotine, which provide a valuable resource to unravel the molecular mechanism underlying nicotine addiction. Through its interaction directly or indirectly with these genes and biological pathways, nicotine evokes multiple effects in the central nervous system.
