An experiment was conducted to determine whether exogenous estradiol-17beta (E2) could restore sexual behavior in castrated rams. The protocol consisted of three sequential 6-wk periods during which rams were studied while 1) intact, 2) bilaterally castrated, or 3) implanted s.c. with two 7.6-cm silastic implants each containing 309+/-16 mg of E2. Rams (classified as female-oriented [FOR, n = 7], male-oriented [MOR, n = 7], or asexual [n = 7]) were subjected to 30-min sexual behavior tests every 2 wk during the ensuing 18 wk. Rams were observed for mounts and ejaculations using two ovariectomized, estrous ewes and two intact males secured in stanchions. Behavioral data were analyzed using the signed rank test, but asexual rams showed no sexual behavior and therefore were not evaluated statistically. Jugular blood was collected prior to castration and at the end of the 18-wk period, and testicular venous (n = 21) and arterial (n = 8) bloods were collected immediately prior to castration. Radioimmunoassay was used to quantify systemic levels of estrone (E1), E2, and testosterone (T) and testicular serum concentrations of oxytocin (OT). Mounting behavior of MOR and FOR declined after castration (P < .05 and P < .10, respectively). Castration reduced the number of ejaculations by FOR (P < .05), but not by MOR (P > .10). Mounting behavior of castrated MOR and FOR was not affected by E2 treatment relative to that observed if castrated only (P > .10). Treatment of asexual rams with E2 did not stimulate sexual behavior in these rams. There were no marked differences (P > .10) among ram groups with regard to serum concentrations of E1, E2, or T prior to castration (overall mean +/- SE, 12.8+/-.7, 7.6+/-.5, and 2,670+/-780 pg/mL, respectively) or any difference (P > .10) in systemic concentration of E1 or E2 among ram groups after rams were implanted with E2 (overall mean +/- SE, 9.7+/-.7 and 9.0 +/-.7 pg/mL, respectively). Serum concentrations of E2 after implantation of the steroid did not differ from those present while rams were intact (P > .10). Testicular venous and arterial serum concentrations of OT were low and did not differ within or between rams. These results suggest that restoration of E2 concentrations to physiological levels in castrated adult rams (regardless of sexual orientation) cannot stimulate or reestablish sexual behaviors to levels observed prior to castration.

Three experiments were conducted, the objectives of which were to 1) examine the effects of exogenous estradiol (E2) and progesterone (P4) on uterine concentrations of oxytocin receptors (OTR) and OTR mRNA, as well as the effect of exogenous P4 on progesterone receptors (PR) during the late luteal phase of the cycle, and 2) ascertain whether chronic E2 treatment of ewes during the cycle would alter prostaglandin F2alpha (PGF2alpha)-induced secretion of luteal oxytocin (OT). In experiment 1, 15 ewes were assigned to a control (n = 5; 2 ml corn oil [CO] s.c. on Days 4-14 of the estrous cycle) and two treatment groups (n = 5 each) receiving either 250 microg E2 s.c. (Days 4-14) or 10 mg P4 s.c. (CO on Days 4-10 and P4 on Days 11-14). Endometria and corpora lutea were removed on Day 15 of the cycle. Mean luteal weights were greater in treated than in control ewes (p < 0.05). Endometrial concentrations of OTR and OTR mRNA were significantly greater in control than in E2- or P4-treated ewes. In experiment 2, five ewes each were treated s.c. with CO or 10 mg P4 on Days 11-14 of the cycle; endometria were then removed on Day 15 for PR assay. Endometrial concentration of PR did not differ between groups. Experiment 3 consisted of 20 ewes assigned to four groups in a 2 x 2 factorial arrangement. Treatment consisted of two dosages of E2 (0 or 250 microg/day) in 2 ml CO and two dosages of PGF2alpha analogue (0 or 125 microg Estrumate). All ewes were injected s.c. with E2 or CO for 11 days as described for experiment 1. On Day 15, all ewes received an i.v. injection of PGF2alpha or saline (Time 0); then jugular blood was collected at frequent intervals for analysis of serum concentrations of OT. PGF2alpha induced a release of OT in control and E2-treated ewes (p < 0.05) compared to the value in saline-treated ewes. Collectively, these data suggest that in cycling ewes, exposure of the uterus to increased concentrations of E2 or P4 causes down-regulation of OTR as a consequence of suppression of the OTR gene. Chronic E2 treatment of ewes during the cycle does not act directly on the ovary to alter the stores of luteal OT.

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