, 2009). Madrigal et al. (2001) also reported that complexes I–III and II–III of mitochondrial respiratory chain were inhibited in rat brain after chronic stress (immobilization for six hours over 21 days). Additionally, Ben-Shachar and Karry (2008) demonstrated reductions in

mRNA and protein of complex I see more subunits NDUFV1, NDUFV2 and NADUFS1 in the postmortem cerebellum from patients with depression. Hroudova and Fisar (2010) using an in vitro study from pig brain, demonstrated that the complex I, II and IV activity decreased with antidepressants and mood stabilizers, suggesting in this study that antidepressants generally act as inhibitors of electron transport chain. Our findings selleck inhibitor also showed an inhibitory effect on the activity of complex I, but contrarily to this, lamotrigine and imipramine increased the activities of complexes II, II-III and IV, suggesting

that the increase in the complexes II, II-III and IV activity may be related, at least in part to compensating the decrease of complex I activity. Such, the effects of lamotrigine and imipramine on the mitochondrial respiratory chain could be positive, taking into account that there is impairment in energy metabolism related to depression (Ben-Shachar and Karry, 2008, Rezin et al., 2009 and Madrigal et al., 2001). A balance between cell death and cell proliferation must be maintained to ensure the health of every human being. Recent findings indicate that approximately one-half of all major human diseases are a first consequence of abnormal apoptosis (Reed, 2002). Neurodegeneration mediated by apoptosis can be initiated by Bax translocation from the cytosol to the mitochondria, where it affects

membrane permeability and permits cytochrome c release and subsequent activation of caspases ( Yang et al., 1995 and Ghribi et al., 2001). Inappropriate apoptosis can cause autoimmune and neurodegenerative disorders, as well as heart disease, while resistance to apoptosis can promote cancer and impede the effectiveness of cancer therapeutics. Our results demonstrate that imipramine and lamotrigine decreased the Bcl-2 expression in the prefrontal cortex, amygdala and hippocampus in the acute and chronic treatments. Peng et al. (2008) showed that 3 μM imipramine treatment significantly up-regulated the mRNA and protein expression and Bcl-2 in day-7 imipramine-treated neural stem cells (NSCs). Huang et al. (2007) also showed that desipramine increased the Bcl-2 expression in day 3 DP-treated NSCs. Another study demonstrated that by the fourteenth day, (but not acute treatment with citalopram), imipramine and amitriptyline in mice had significantly elevated the hippocampal Bcl-2 protein expression as compared to vehicle treated animals.