Chronic treatment with coenzyme Q10 reverses restraint stress-induced anhedonia and enhances brain mitochondrial respiratory chain and creatine kinase activities in rats.

Several recent studies suggest a close link between mitochondrial dysfunction and depression. Coenzyme Q10 (CoQ10) is a mobile electron carrier in the mitochondrial respiratory chain (MRC) with antioxidant and potential neuroprotective activities. This study investigated the effect of chronic administration of CoQ10 (50, 100, and 200 mg/kg/day, intraperitoneally, for 4 weeks) on anhedonia and on the activities of MRC complexes and creatine kinase in the frontal cortex and hippocampus of Wistar rats subjected to chronic restraint stress (CRS, 6 h × 28 days). Exposure to CRS-induced anhedonic-like behavior (decreased sucrose preference), reduced body weight gain and food intake, increased adrenal gland weight, and altered the activity of the MRC complexes in the brain areas tested. CoQ10 dose-dependently antagonized CRS-induced depressive behavior by increasing sucrose preference (reversal of anhedonia), body weight, and food intake and reducing adrenal gland weight. CoQ10 also enhanced the activities of MRC complexes (I-IV) and creatine kinase in the frontal cortex and hippocampus. Thus, the reversal of CRS-induced anhedonia may be partially mediated by amelioration of brain mitochondrial function. The findings also support the hypothesis that brain energy impairment is involved in the pathophysiology of depression and enhancing mitochondrial function could provide an opportunity for development of a potentially more efficient drug therapy for depression.