Involvement of dopamine receptors in cocaine-induced genital reflexes after paradoxical sleep deprivation

Abstract

Previous work has demonstrated that paradoxical sleep deprivation (PSD) potentiates cocaine-induced genital reflexes in male rats. To examine the possibility that this effect might involve alterations in binding to the DA transporter (DAT), we examined [ 3H] WIN 35,248 binding in brain after 96 h of PSD. No changes were found in any of the 11 brain regions examined. Since we had previously identified changes in D 2 receptor binding after PSD, we next examined the effects of DA receptor subtype antagonists on cocaine-induced reflexes in sleep-deprived rats. Separate groups of PSD rats received saline, haloperidol (0.4, 0.8 or 1.6 mg/kg), SCH 23390 (0.25, 0.5, 1 mg/kg) or sulpiride (50, 100, 200 mg/kg) 60 min prior to acute cocaine (7 mg/kg). In saline pretreated rats, cocaine-induced penile erection (PE) in 100% of SD rats. This percentage was not significantly reduced by haloperidol at any dose, but was significantly reduced in rats pretreated with SCH 23390 (1 mg/kg) or sulpiride (100 or 200 mg/kg). In addition, acute cocaine-induced ejaculation in 80% of SD rats. This effect was not affected by haloperidol at any dose, but was significantly reduced by all doses of SCH 23390 and by the 200 mg/kg dose of sulpiride. These results suggest that the potentiating effects of cocaine on penile erection and ejaculation are likely due to PSD-induced changes in DA postsynaptic receptor sensitivity rather than alterations in DA transporter. They further suggest that both D 1 and D 2 receptors may play a role in these effects.