coenzyme q10 suppression of cue-related reinstatement through cognition improvement and hippocampal increase in bdnf expression in morphine-dependent male rats

Introduction: opioid dependence significantly disrupts cognitive activities such as learning and memory, which may be the reason for a return to drug use. morphine (mor) can increase oxidative damage in the brain. we aim to investigate the effect of coenzyme q10 (coq10) on cognitive impairment, cue-related reinstatement, and expression of brain-derived neurotrophic factor (bdnf) in mor-dependent rats.methods: in this study, 40 male wistar rats (200-220 g) were divided into 5 experimental groups (n=8) as follows: oil group, mor+oil group, mor+coq10-100 group, mor+coq10-200 group, and mor+coq10-400 group. the rats were administered increasing doses of mor (25 to 100 mg/kg, sc) once daily. after 21 days of addiction, coq10 treatment is administered by gavage at doses of 100, 200, and 400 mg/kg once daily for one month. coq10 is dissolved in 1 ml of sesame oil and administered. behavioral assessments were performed using a novel object recognition (nor) test, working memory in the y-maze, social interaction, and conditioned place preference (cpp). the expression of bdnf was assessed in the hippocampus through immunohistochemistry. results: treatment with coq10 at a dosage of 100, 200, and 400 mg/kg within 4 weeks resulted in a significant improvement in the nor task (p<0.01, p<0.001), working memory in the y-maze (p<0.01, p<0.001), social interaction (p<0.001), cue-related reinstatement in the cpp (p<0.01, p<0.001) and significantly increased expression of bdnf (p<0.001) in the hippocampus of male rats.conclusion: coq10 could improve cognitive impairment and reduce reinstatement in mor-addicted male rats. histologic examination confirmed the neuroprotective effects of coq10 in the hippocampus. coq10 could be a potential therapeutic agent for mor-induced cognitive impairment and relapse.