Although these findings further supported the potential role of mtDNA mutations/polymorphisms in the pathophysiology of bipolar disorder, it is still an open question whether or not mtDNA mutations in the brain can cause bipolar disorder. Thus, we planned to generate an animal model of accumulating mtDNA deletions in the brains. Zhang et al. (2003) had reported transgenic mice carrying heart-specific mutant Polg, showing heart failure. We attached a neuron-specific promoter of CAMKA to the same mutant to assess the behavioral phenotype without the effect of somatic symptoms (Kasahara et al., 2006).