Sham OVX Research Articles

Ovarian Steroid Regulation of Pulsatile Luteinizing Hormone Release During Early Gestation in the Rat

Abstract The object of this study was to examine ovarian regulation of pulsatile luteinizing hormone (LH) secretion during early gestation. This was done primarily by analyzing pulsatile LH release in rats that were either sham ovariectomized (OVX) on Day 7 of pregnancy, implanted with empty Silastic capsules, and bled on Day 8, or OVX on Day 7, immediately implanted with Silastic capsules producing plasma levels of estradiol and/or progesterone characteristic of Day 7 to 8 of pregnancy, and bled on Day 8. In addition, the role of progesterone in regulating pulsatile LH secretion was also examined by administration of the progesterone receptor antagonist, RU486, on Day 7 and examining pulsatile LH release on Day 8 of pregnancy. OVX caused a marked increase in LH pulse amplitude and frequency within 24 h. Replacement with physiological plasma levels of estradiol or progesterone alone had no suppressive effect on this OVX-induced increase in pulsatile LH secretion. Restoration of physiological plasma levels of both estradiol and progesterone returned LH pulse amplitude to values seen in sham OVX controls, and prevented the OVX-induced increase in LH pulse frequency. The group mean LH pulse frequency tended to be less in estradiol + progesterone-treated rats than in sham OVX controls, but this difference was not statistically significant. RU486 blocked uterine progesterone receptors as evidenced by endometrial hemorrhaging. In agreement with the OVX + steroid replacement data, RU486 administration also resulted in increases in LH pulse amplitude and frequency. These data demonstrate that the frequency and amplitude of LH pulses on Day 8 of gestation are held in check by negative feedback signals coming from the ovary. Neither steroid alone exerts any suppressive influence over pulsatile LH secretion during early gestation, but both steroids acting together exert a prominent negative feedback regulation on the pulsatile LH release process.

Changes in hypothalamic catecholamine levels in relation to season, ovariectomy, and 17β-estradiol replacement in the catfish, Clarias batrachus (L.)

In female Clarias batrachus, hypothalamic levels of noradrenaline (NA) and dopamine (DA) exhibited seasonal changes during different phases of the annual reproductive cycle. The NA level was high during gonadal recrudescence (prespawning and spawning phases) and low during gonadal quiescence (postspawning and resting phases). A reverse trend was noticed in the DA level. After 3 weeks of ovariectomy (Ovx), the catecholamine (CA) levels were elevated significantly in the preparatory, prespawning, and spawning phases and were unaltered in the postspawning season. Administration of 17β-estradiol (E 2, 1.0 μg/g BW) to 3-week Ovx fish resulted in both seasonal and differential effects on the CA levels. The NA level was significantly elevated in the preparatory phase, decreased in the prespawning and spawning phases, and remained unaltered in the postspawning season. The DA level was restored by the steroid treatment in the preparatory phase, but registered a significant elevation in the prespawning and spawning phases. In the prespawning phase, Ovx induced a significant elevation of the hypothalamic NA level after 2, 3, and 4 weeks, but was significantly low after 5 weeks. The DA level registered a significant increase after 2, 3, and 5 weeks of Ovx. Administration of E 2 to 3-week Ovx fish elicited dose-dependent responses on CA levels. The administration of a low dose of E 2 (0.05 μg) caused a significant elevation of the NA level, while the 0.1 μg dose did not alter the amine level in comparison to that of the Ovx vehicle group. The higher doses (0.5 and 1.0 μg) of E 2, however, decreased the NA level significantly below that of the sham vehicle and Ovx vehicle groups. The DA level was unchanged in the 0.05-μg group and registered a significant increase at 0.1, 0.5, and 1.0 μg/g doses of E 2. The results suggest that changes in the circulating level of E 2 may influence hypothalamic CA which, in turn, may modulate the secretion of gonadotropin from the pituitary.

Effects of Neonatal Ovariectomy upon <sup>3</sup>H-Estradiol Uptake by Target Tissues of Androgen-Sterilized Female Rats

Tissue distributions of radioactivity were studied at 2, 4 and 6 h after intravenous injection of 3H-estradiol-17 beta (48.6 ng/100 g b.w.) in 4 groups of 10 or 11 adult female rats with the following neonatal treatments: Control = sham ovariectomy (ovx) on day 1, oil injection on day 5 (n = 10); ovx = ovx on day 1, oil on day 5 (n = 11); TP = sham ovx on day 1, 30 micrograms testosterone propionate (TP) on day 5 (n = 10); ovx-TP = ovx on day 1, 30 micrograms TP on day 5 (n = 11). Neonatal TP treatment significantly hastened vaginal opening in all animals. After ovariectomy, vaginal opening occurred in 20/22 rats regardless of hormonal treatment; ovariectomy did not significantly affect the time of vaginal opening in these 20 animals. All ovariectomized animals had diestrous vaginal smears after puberty, all controls cycled normally and all of the TP group used for the uptake part were in persistent vaginal estrus (sequence of vaginal smears with 70% or more containing no leukocytes) confirmed by ovarian histology to be anovulatory (11/13 injected). 72 h prior to radioisotope injection, intact females in the above groups were ovariectomized and the neonatally ovariectomized were sham operated. Tissue radioactivity was extracted from the anterior, middle and posterior hypothalamus, hippocampus, amygdala, cerebrum, anterior pituitary, uterus and plasma. Neonatal ovariectomy raised 3H-estradiol concentrations in all tissues, except hippocampus and anterior pituitary, suggesting an increase in nonspecifically bound hormone. Neonatal TP decreased 3H-estradiol concentrations in the anterior and middle hypothalamus and uterus only, in both the intact and ovariectomized group, demonstrating a selective effect of neonatal TP upon subsequent development of estrogen binding capacities of target tissues that is independent of the ovaries.