Site-specific opioid receptor blockade allows prepubertal guinea pigs to display progesterone-facilitated lordosis

Ovariectomized (OVX) juvenile guinea pigs (approximately 3 weeks old) rarely display steroid-induced sexual receptivity. Systemic administration of the opioid receptor antagonist naloxone enhances the display of progesterone-facilitated lordosis in prepubertal females, suggesting that endogenous opioids tonically inhibit the expression of sexual receptivity at this age. This study was designed to ascertain the neural site(s) at which naloxone injection would stimulate lordosis in juvenile guinea pigs. Hartley guinea pigs were OVX at 10-11 days of age and 2-6 days later implanted with bilateral cannulae aimed at the medial preoptic area/anterior hypothalamus (MPOA/AH), ventrolateral hypothalamus/ventromedial hypothalamus (VLH/VMH), or mesencephalic central gray (MCG). At 21-23 days of age, following administration of estradiol benzoate (10 microgram(s)) and progesterone (0.5 mg), naloxone (100 ng/side) or 0.9% saline was injected through the cannulae and the guinea pigs were tested for the display of lordosis. The MPOA/AH was the only site at which application of naloxone reliably elicited lordosis (87% positive response vs 12% for saline). Few females (< 17%) displayed lordosis following injections of naloxone or saline into the VLH/VMH or MCG. A second experiment demonstrated that the stimulation of lordosis following MPOA/AH naloxone application was prevented by prior injection of the opioid agonist morphine (500 ng/side) at the same site. These data support the hypothesis that endogenous opioids acting in the MPOA/AH, but not the VLH/VMH or MCG, tonically inhibit the display of progesterone-facilitated lordosis in prepubertal guinea pigs.