Drug-induced neuroplasticity involves some common molecular and cellular changes of the neurocircuitries (Hyman & Malenka, 2001; Kauer & Malenka, 2007; Koob & Volkow, 2010), such as dopaminergic transmission in mesolimbic system, and corticotropin-releasing factor and norepinephrine systems in the extended amygdale. We have also observed significant overlap of gene expression and pathway alteration in both cocaine- and alcohol-addicted brains. Among the 48 differentially expressed genes (FDR<0.2) in the alcoholics, 29 were common to cocaine addicts and in each case the change was in the same direction. More strikingly, for the 11 most significantly differentially expressed genes (FDR<0.05) in alcoholics, 9 were also altered to the same degree in the cocaine addicts, suggesting shared pathways impacted by both cocaine and alcohol in neuronal adaptation. It is apparent that these commonly affected protein-coding genes (Fig. 10.1C) play important roles in neuronal functions. They include CDR1, a cerebellar degeneration-related protein; LRCH4, a leucine-rich repeat-containing neuronal protein; CACNB2, a subunit of voltage-gated calcium channel and involved in neuronal functions; and FAM123A (AMER2), a member of the gene family involved in neurogenesis (Comai, Boutet, Neirijnck,
