Objective: Several studies have reported that Clomipramine hasthe ability to suppress male rat sexual behavior. Literature indicatesthat the activation of brain D2 receptors causes facilitation ofpenile erection, and a number of reports have indicated dopamine'sinvolvement in sexual function. Hence this study was undertakento investigate the effect of Amantadine, a dopamine agonists onthe Clomipramine induced sexual dysfunction. Methods: The study subjects involved a total of 48 males and 48females, 4 months old Sprague-Dawley albino rats, all housed ina group of six males and females separately in plexi glass cages inan acclimatized colony room (25±0.50C) maintained on a 12/12hr light/dark cycle. The male rats were randomly divided into fourgroups of 12 male rats each. Group I served as controls. Group II,III, and IV were treated with Amantadine (9 mg/kg body weight,p.o) 30 min, prior to the treatment with 13.5 mg/kg, 27 mg/Kgand 54 mg/Kg bodyweight p.o of Clomipramine respectively for 60days. The control group received vehicle 1 ml/kg p.o. The sexualbehavior of the male rats was observed to determine the followingparameters: mount latency, intromission latency, ejaculationlatency, post ejaculatory pause, and intromission frequency. Aswell as the sexual behavior; serum testosterone and histopathologyof the testes were also investigated in this study. Results: The results indicate that Amantadine in all aspectsfailed to antagonize Clomipramine induced sexual dysfunction inmale rats. Even the sexual competence of male rats treated with1/2 therapeutic dose (TD) of Clomipramine failed to regain theirsexual competence in the presence of Amantadine. Testiculardamage and decline in testosterone levels continued in the presenceof Amantadine. Conclusion: Overall, the results suggest that Amantadine couldnot be a safe antidote to antagonize Clomipramine induced sexualdysfunction.