Nicotine is the primary addictive component of tobacco smoke (Dani and Harris 2005; Wonnacott et al. 2005). Through interactions with nicotinic acetylcholine receptors (nAChRs) in the central nervous system (CNS), nicotine modulates various genes and cellular pathways in target neurons. For example, nicotine upregulates the expression of immediate early genes such as c-Fos, c-Jun, Nurr77, and Egr1 (Ichino et al. 1999; Ichino et al. 2002; Shim et al. 2001). Also, mitogen-activated protein kinase (MAPK) signaling, phosphatidylinositol phosphatase signaling, growth factor signaling, and ubiquitin-proteasome pathways are modulated by chronic nicotine treatment (Konu et al. 2001; Li et al. 2004; Tang et al. 1998). Further, animal studies indicate that nicotine, like other drugs of abuse, stimulates the mesocorticolimbic dopamine system in the outer shell of the nucleus accumbens (NA) (Pontieri et al. 1996; Robbins and Everitt 1999) and modulates the release of other neurotransmitters such as norepinephrine, serotonin, acetylcholine, glutamate, and GABA (Barik and Wonnacott 2006; MacDermott et al. 1999; Schilstrom et al. 2000; Vizi and Lendvai 1999; Wonnacott 1997). Through its interaction directly or indirectly with these genes, pathways, and neurotransmitter
