ABSTRACT
Several studies have reported that Clomipramine has the ability to suppress male rat sexual behavior. Literature indicates that the activation of brain D2 receptors causes facilitation of penile erection, and a number of reports have indicated dopamine's involvement in sexual function. Hence this study was undertaken to investigate the effect of Amantadine, a dopamine agonists on the Clomipramine induced sexual dysfunction. The study subjects involved a total of 48 males and 48 females, 4 months old Sprague-Dawley albino rats, all housed in a group of six males and females separately in plexi glass cages in an acclimatized colony room [25 +/- 0.5[degree sign]C] maintained on a 12/12 hr light/dark cycle. The male rats were randomly divided into four groups 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/Kg and 54 mg/Kg bodyweight p.o of Clomipramine respectively for 60 days. The control group received vehicle 1 ml / kg p.o. The sexual behavior of the male rats was observed to determine the following parameters: mount latency, intromission latency, ejaculation latency, post ejaculatory pause, and intromission frequency. As well as the sexual behavior; serum testosterone and histopathology of the testes were also investigated in this study. The results indicate that Amantadine in all aspects failed to antagonize Clomipramine induced sexual dysfunction in male rats. Even the sexual competence of male rats treated with 1/2 therapeutic dose [TD] of Clomipramine failed to regain their sexual competence in the presence of Amantadine. Testicular damage and decline in testosterone levels continued in the presence of Amantadine. Overall, the results suggest that Amantadine could not be a safe antidote to antagonize Clomipramine induced sexual dysfunction