Effect of 5α-dihydrotestosterone and flutamide on the facilitation of lordosis by LHRH and naloxone in estrogen-primed female rats

Abstract

Although 5α-dihydrotestosterone (DHT) is a potent inhibitor of lordosis behavior in ovariectomized estrogen-primed female rats, the mechanism(s) by which this steroid has this action is unknown. The present experiments sought to determine whether DHT inhibits lordosis by preventing the known facilitatory actions of luteinizing hormone-releasing hormone (LHRH), naloxone, and Substance P on lordosis. Lordosis behavior was examined in ovariectomized, estrogen-primed rats prior to or 30, 60, 90, and 180 min following intracerebroventricular (ICV) infusion of LHRH (500ng), naloxone (1 μg), Substance P (1 μg), or saline and 0.01 N acetic saline vehicles, and the effects of DHT (2.5 mg/rat) following similar treatment were examined. In Experiment 1, LHRH and naloxone increased lordosis within 30 min after infusion, while Substance P and the saline or acetic saline vehicles had no effect. Treatment with DHT in combination with estrogen prevented the facilitation of lordosis by LHRH and naloxone. In Experiment 2, ovariectomized, estrogen-primed females shown to be responsive to LHRH during a first screening test were tested for lordosis after receiving either DHT or DHT in combination with the androgen receptor antagonist, Flutamide (7.5 mg/injection × 3). Again, DHT prevented the facilitatory action of LHRH; however, Flutamide did not counteract that effect. In Experiment 3, Flutamide did not counteract the inhibitory effect of DHT on estrogen and progesterone-induced lordosis. These results demonstrate that the inhibitory effect of DHT cannot be overridden by neuroactive peptides which themselves stimulate receptivity. It seems unlikely that DHT inhibits lordosis either by interfering with the behavioral action of these peptides or by activation of the androgen receptor.