The effect of hysterectomy on hormone-induced lordosis behavior in hamsters
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Low doses of estradiol benzoate (2.5-10.0 μg/day X 5) inhibited the production of erythropoietin (Ep) in female rats exposed to various intensities of hypoxia. This was not attributable to the presence of either residual estradiol, or an inhibitor of Ep in plasma samples, since these plasmas had no inhibitory effect on Ep simultaneously injected into assay mice. Although normal females produced less Ep in response to hypoxia than normal males, ovariectomized rats showed a response equal to males. Estradiol treatment of ovariectomized animals lowered their Ep response to hypoxia down to the level of intact females. Only the largest dose employed (10.0 μ/day) had some inhibitory effect on Ep production in hypoxic males. (Endocrinology92: 358, 1973)
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Z‐Bisdehydrodoisynolic Acid (Z‐BDDA) has been described as highly estrogenic, and a selective estrogen receptor modulator, based exclusively on uterotrophic activity in female rats. Exploring possible neuroprotective effects of Z‐BDDA, we thought it important to determine whether Z‐BDDA has estrogenic effects in the brain. Accordingly, female Sprague‐Dawley rats were ovariectomized (ovx) under isofluorane anesthesia and assigned to various steroid treatment protocols intended to induce sexual receptivity. Z‐BDDA (300ug/rat or 30ug/rat) or Estradiol benzoate (10 ug/rat) was administered (sc) two weeks following ovx and some rats were also given Progesterone (1mg/rat) 48 hours later. Lordosis behavior was assessed by placement of female rats in an arena containing a sexually mature male rat. Mount attempts by the male and lordotic responses in the females were recorded. Results showed that female rats treated with either Z‐BDDA or Estrogen (followed or not by Progesterone) exhibited profound receptivity assessed by display of lordosis in response to male mount attempts. Thus, this study further establishes the estrogenicity of Z‐BDDA and demonstrates a positive feedback effect on the central nervous system that appears to parallel the peripheral (uterotrophic) effects of the compound. Supported by the SIU School of Medicine Center for Integrated Research in Cognitive and Neural Sciences. Grant Funding Source : None
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Altered Negative Feedback Response to Ovariectomy and Estrogen in Prepubertal Restricted-diet Rats 1
Studies were conducted to explore the hypothesis that the delayed sexual maturation of female rats induced by reduced food intake (R) may result partially from an altered negative feedback response to estrogen. Animals were placed on 60% of normal food intake at 20 days of age. Controls (C) were fed ad libitum. Rats were used for three different experiments at 31-32 days of age. In Experiment I, rats were ovariectomized (OVX) and injected subcutaneously for 4 days with varying doses of estradiol benzoate (EB). They were killed the day after the last injection. In Experiment II, rats were ovariectomized and killed in groups at 4, 12, 24, 48, 72, and 120 h after OVX. In Experiment III, they were castrated and 1 wk later received a single injection of 0.5 microgram EB. Groups were killed at 1, 2, 4, 8, and 24 h after injection. Sera from all experiments were assayed for follicle-stimulating hormone (FSH), luteinizing hormone (LH), and prolactin. Results of Experiment I indicate that the efficacy of EB for suppressing LH, but not FSH, secretion is increased significantly in R rats. In Experiment II, OVX resulted in a delayed increase in serum LH, but not FSH, concentrations of R rats when compared to C animals. Results of Experiment III indicate a delayed, but more prolonged, suppression of LH secretion by EB in R rats when compared to C rats. Prolactin secretion, on the other hand, increased earlier in R rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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Effects exerted by localized hypothalamic and hypophysial implants of minute amounts of estradiol benzoate on pituitary and plasma LH were studied with the use of the ovarian ascorbic acid depletion method (OAAD). In control ovariectomized rabbits the pituitary LH content measured 0.53 ±0.05 μg/mg- When estrogen was implanted in the posterior median eminencebasal tuberal region of the hypothalamus (PME), the pituitary LH content was reduced to less than 0.1 μg/mg in 5 of 7 rabbits. However, when estrogen was implanted in other parts of the hypothalamus, it failed to depress pituitary LH (0.51 ±0.06 μg/mg). With estrogen in the anterior hypophysis, the pituitary LH content was also somewhat lowered (0.34 ±0.03 μg/mg). The castration level of plasma OAAD, an indicator of plasma LH content, was 21.6 ± 3.3 % as compared with the normal (noncastrate) level of 5.8 ±0.9%. Estrogen implants in PME inhibited the postcastration elevation in plasma OAAD (9.1 ±3.4%), whereas implants in other parts of the hypothalamus were ineffective (plasma OAAD, 24.1 ±2.5%). The plasma OAAD level in animals with estrogen implanted in the anterior hypophysis was even higher (34.2 ±1.8%) than in the castrate controls. Estrogen implantation into PME resulted in a doubling of the weight of the hypophysis, whereas similar effects were not observed following implantation into other parts of the hypothalamus or directly into the anterior hypophysis. The results indicate that estrogen acts on PME in such a way as to inhibit synthesis of pituitary LH and thereby to prevent the postovariectomy rise in plasma LH, while at the same time stimulating hypertrophy of the hypophysis. Acting directly on the anterior hypophysis, estrogen appears to activate release of LH into the circulation, where it is reflected in elevated plasma OAAD. (Endocrinology75: 579, 1964)
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There are data indicating that stress-induced prolactin (PRL) release is blunted in the lactating rat like the release of other stress-associated hormones. In this experiment, the PRL release evoked by administration of estrogen, which is another principal stimulus for PRL release, was examined in ovariectomized lactating rats 8-15 days after delivery. Estradiol benzoate (EB, 20 µg) injections into ovariectomized nonlactating rats induced a PRL surge starting between 13:00 and 15:00 h with a peak at 17:00 h 2 days after the treatment, whereas the EB-induced PRL surge was absent in ovariectomized lactating rats separated from their pups at 09:00 h on the day or in mothers without separation from their pups. Injection of either thyrotropin-releasing hormone (TRH; 10 µg/kg) or pimozide (0.5 mg/kg) elevated serum PRL concentrations similarly in lactating and nonlactating rats when examined just before the beginning of the expected estrogen-induced PRL surge. Thus, the main cause for the reduced PRL response to estrogen in lactating rats seems not to be in the pituitary gland but in the brain. Progesterone, which is know to induce a PRL surge in ovariectomized estrogen-primed rats by acting on the mediobasal hypothalamus, also failed to evoke a PRL surge in lactating rats. Recovery from the inhibitory influence of suckling on PRL response to EB followed a time course similar to that observed in response to immobilization stress or to morphine injection; estrogen-induced PRL surge started to recover at 6 days and was almost fully recovered 8 days after weaning. These facts indicate that suckling stimuli may cause functional alterations in the neural systems responsible for PRL release, resulting in refractoriness of the PRL response to ovarian steroids.
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The role of estrogen and progesterone in facilitating the proestrous release of LH was examined in 4-day cyclic rats. Ovariectomy at 1000 hr diestrous day 2 eliminated the expected proestrous plasma LH surge. Administration of either 1.0, 10.0 or 50 μg estradiol benzoate (EB)/100 g body wt (1000 hr diestrous day 2) re-established gonadotropin release in these animals, with the intermediate dosage being most effective. However, peak plasma LH concentrations did not approach normal proestrous levels, and the rates of release were abnormally slow and more sustained. On the other hand, 10.0 μg 17β-estradiol (E2)/100 g body wt was more effective in eliciting the discharge of normal patterns and concentrations of pituitary LH. Progesterone (2 mg), administered at 0930 hr proestrous potentiated the plasma LH response in estrogentreated ovariectomized animals and also synchronized the timing of the gonadotropin surge. Estrogen replacement alone failed to produce a rise in plasma LH on proestrus in adrenalectomized- ovariectomized animals. When progesterone was administered to these rats following estrogen priming, elevated proestrous plasma LH concentrations were again observed. These results suggest that progesterone is required to act synergistically with estrogen to facilitate the proestrous surge of LH in the rat. The most likely source of this progesterone is the adrenal gland. (Endocrinology93: 694, 1973)
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