In contrast to the amygdala and hippocampus, in the NA, mitochondrial electron transport genes were downregulated by nicotine, as evidenced by the suppression of Mt-co1, Mt-cyb, and Mt-nd6. The expression of genes related to other functions also was reduced. In the PFC, we detected the induction of genes involved in electron transport (e.g., Atp5j, Mt-co1, Mt-cyb, and Mt-nd6), protein modification or transport (Canx, Nedd4, and Stx12), and signal transduction (Ywhae). In the striatum, some genes were suppressed by nicotine, such as Mt-nd6, secretogranin II (Scg2), and voltage-gated sodium channel type III beta (Scn3b), whereas others were induced, such as insulin-like growth factor binding protein 5 (Igfbp5), nuclear receptor subfamily 4 group A member 1 (Nurr1), and Stathmin 1 (Stmn1). Among the genes detected in the VTA, those related to electron transport (e.g., Atp5j, Mt-co1, Mt-cyb, and Mt-nd6), as well as mRNA processing (e.g., heterogeneous nuclear ribonucleoprotein H1 [Hnrph1], PRP18 pre-mRNA processing factor 18 homolog [Prpf18], and RNA-binding motif protein 16 [Rbm16]) were upregulated. Whereas a number of transcription regulators such as forkhead box A1 (Foxa1), mortality factor 4 like 1
