Systemic or intracranial apomorphine increases copulation in long-term castrated male rats.

Testosterone or its estrogenic metabolite is thought to be necessary to activate male rat sexual behavior. However, systemic injections of dopamine agonists, alone or in combination with exogenous testosterone, can partially restore copulatory behavior during the prolonged period of its postcastration decline. The present experiments tested the ability of the dopamine agonist apomorphine, injected systemically or into the medial preoptic area (MPOA), to restore copulation in long-term castrates that had failed to copulate on two successive weekly tests. In Experiment 1, systemic injections of apomorphine increased the number of mounts and intromissions in castrated males, compared to vehicle. In castrates given subthreshold testosterone propionate (TP), apomorphine increased the number of mounts. In Experiment 2, microinjections of apomorphine into the MPOA increased the number of mounts in animals without TP. Subthreshold TP had no significant effects in either experiment, either alone or interacting with apomorphine. These results suggest that stimulation of dopamine receptors can partially restore copulation, even after its virtual elimination. Furthermore, dopamine receptors in the MPOA may contribute to sexual arousal in long-term castrates.

D2/D1 ratio in the medial preoptic area affects copulation of male rats.

The D1/D2 dopamine agonist apomorphine, microinjected into the medial preoptic area (MPOA), facilitates male rat sexual behavior and the D1/D2 antagonist cis-flupenthixol in the MPOA impairs it. The present study investigated the roles of D1 and D2 receptors in the regulation of copulation by microinjecting drugs selective for these receptors into the MPOA. The D2 agonist LY-163502 delayed the onset and slowed the rate of copulation and also reduced the number of vaginal intromissions required to trigger ejaculation (reduced ejaculatory threshold). The D1 agonist SKF-82526 had no effect, either alone or together with LY-163502. The D1 antagonist SCH-23390 delayed the onset of copulation and decreased ejaculatory threshold, as had the D2 agonist. A low dose of the D2 agonist alone and together with the D1 antagonist delayed the onset of copulation and reduced ejaculatory threshold; the combination of drugs was more effective than LY-163502 alone. Only the combination of drugs slowed the rate of copulation and delayed the resumption of copulation after an ejaculation. Thus, increasing the D2/D1 ratio in the MPOA, by selective stimulation of D2 and/or antagonism of D1 receptors, delays the onset of copulation and reduces ejaculatory threshold, possibly by altering autonomic control of penile reflexes.