Apomorphine-induced disruption of paced mating behavior in female rats is attenuated by eticlopride, a D2 receptor antagonist, but not SCH 23390, a D1 receptor antagonist

Dopamine is linked to sexual motivation and genital arousal in female rats. The present study investigated the effects of systemic apomorphine, a dopamine receptor-type 1 (D1) and -type 2 (D2) agonist, on no contact partner preference and paced mating behavior. Ovariectomized, hormone-primed, sexually experienced female rats received 80 μg/kg apomorphine or vehicle 10 min before a partner preference test followed immediately by a paced mating test (Experiment 1). Partner preference did not differ by treatment. However, apomorphine-treated rats exhibited significantly longer contact-return latencies to mounts, intromissions, and ejaculations, greater likelihood of withdrawal after mounts and intromissions, longer intervals between intromissions, reduced time with male, and fewer proceptive behaviors compared to rats receiving vehicle. To test whether effects of apomorphine on paced mating behavior were mediated primarily by D1 or D2 receptors, rats were pretreated with 25 μg/kg eticlopride, a D2 antagonist, or 25 μg/kg SCH 23390, a D1 antagonist, 10 min before receiving 80 μg/kg apomorphine. Rats were then tested for partner preference and paced mating as in Experiment 1. Eticlopride pretreatment attenuated effects of apomorphine; eticlopride → apomorphine-treated rats displayed significantly shorter contact-return latencies to intromission, reduced percentage of exit after mounts, shorter intervals between intromissions, decreased time with male, and more proceptive behaviors relative to saline → apomorphine-treated rats. Effects of apomorphine were not altered by SCH 23390 pretreatment. Apomorphine only affects sexual motivation when mating is possible, indicating that dopamine manipulation influences the physiology that supports behavioral response to sexual stimulation.