Sex differences in the induction of cytosolic progestin receptors (CPR) by estrogen priming were correlated with the sex differences in behavioral responses. We evaluated the temporal relationship between CPR in several brain regions and pituitary and the timecourse of 17P-estradiol (E,) activation of female sexual behavior in gonadectomized male and female rats implanted with sribcutaneous E, Silastic capsules for 6 h, 24 h and 48 h. Both CPR levels and mating behavior increase monotonically with the time 0; E, exposure. Induction of CPR was observed in the periventricular region of the preoptic area (PVPOA), arcuate nucleus (ARC), ventromedial nuclei (VMN) and pituitary in both sexes. A small induction of CPR was found in parietal cortex. The VMN in female rats showed a significant E,-induced CPR increase a t all times of exposure, while in male rats this induction was only significant after 24 h. Significant sex differences in absolute CPR levels and E,-induced receptors were found in the following structures: VMN, 18 h after 6 h of E, treatment and after 24 h and 48 h of continuous E, exposure; PVPOA, only after 48 h of continuous E, exposure; ARC at 24 h and 48 h; and pituitary after all E, treatment. Mating behavior was tested under two conditions: E, alone (2 h after removal of E, capsules) and E,+ progesterone (2 h after a progesterone injection given 10 min after concluding the first test). Receptivity was first observed after 24 h E, exposure in female rats, whereas in male rats a small response appeared only after 48 h of E, exposure. After progesterone priming, the time of E, exposure necessary for expression of female sexual behavior was reduced to 6 h in females and 24 h in males. The appearance of mating behavior appears to follow that of inducible CPR in the VMN in both sexes. In addition, the CPR levels associated with the first receptivity either by male rats (16.6 fmol/mg protein) or female rats (15.3 fmol/mg protein) are very similar suggesting the presence of a threshold level controlling the expression of feminine sexual behavior. It is likely that in!iibitory neural input plays a role in determining the threshold level of E,-induced CPR, which is sufficient to trigger lordosis behavior.Thc sequential secretion of ovarian steroid 17B-estradiol (E,) and Progesterone (P) during the estrous cycle, interact synergistically controlling the onset, quality and duration of the female rat sexual behavior (1, 2). The gonadal steroid effect on this behavior expression can be mimicked in ovariectomized female rats by trei tment with physiological doses of estrogens followed by P priming (3, 4).In male rats the expression of female sexual behavior is not normally expressed. However, chronic administration of estradiol kilxoate (EB) in various dosages to castrated males resulted in a moderate increase of the lordosis behavior (5-7) which is poorly or not at all increased by P treatment (8,9). The sex differences in the response to E, and P treatment have been attributed to diff'crences in the est...