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PubMed1994

Mono-(2-ethylhexyl) phthalate suppresses estradiol production independent of FSH-cAMP stimulation in rat granulosa cells.

Di-(2-ethylhexyl) phthalate (DEHP) exposure suppressed preovulatory granulosa cell estradiol production in adult cycling rats. The active metabolite of DEHP, mono-(2-ethylhexyl) phthalate (MEHP), suppressed follicle-stimulating hormone (FSH)-stimulated cAMP and progesterone production in cultured rat granulosa cells. To examine how DEHP altered granulosa cell estradiol production, the effects of MEHP were studied in cultures of rat granulosa cells. Granulosa cells were obtained from DES-implanted 25-day-old female Fisher 344 rats and exposed in culture to various concentrations of MEHP (0 to 400 microM) in DMSO. Granulosa cells were stimulated with FSH, 8-bromo cyclic adenosine monophosphate (8br-cAMP), a stable cAMP analog, and various concentrations of testosterone. Estradiol production was measured by standard radioimmunoassays and normalized to cell protein. MEHP suppressed estradiol in a concentration-dependent manner whether granulosa cells were stimulated by FSH or 8-br cAMP. Therefore, MEHP suppressed estradiol independent of its suppression of the FSH-cAMP pathway and, thus, suppressed aromatase conversion of testosterone to estradiol. MEHP (100 microns) decreased the maximum velocity of aromatase in cells supplied with increasing concentrations of testosterone. However, MEHP did not alter the velocity or affinity of microsomal aromatase isolated from adult virgin Sprague-Dawley rat ovaries. Therefore, MEHP altered the absolute amount or availability of aromatase in granulosa cells. Decreased aromatase in granulosa cells would explain decreased estradiol concentrations from DEHP exposure in vivo.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1996

In vivo modulation of 17 beta-estradiol-induced vitellogenin synthesis and estrogen receptor in rainbow trout (Oncorhynchus mykiss) liver cells by beta-naphthoflavone.

Vitellogenesis or egg yolk production represents a key estrogen initiated process in oviparous vertebrates which is crucial for oocyte maturation. Previous in vitro studies have shown that cytochrome P4501A1 (CYP1A1)-inducing compounds such as beta-naphthoflavone (betaNF) modulate 17 beta-estradiol-induced vitellogenin (Vg) synthesis in primary cultures of juvenile rainbow trout liver cells. In this study, treatment of juvenile trout with 0.5 mg/kg 17 beta-estradiol plus either 25 or 50 mg/kg betaNF confirmed in vivo that betaNF may depress Vg synthesis by the liver. Alternatively, trout treated with 0.5 mg/kg 17 beta-estradiol plus 12.5 mg/kg betaNF or 5 mg/kg 17 beta-estradiol plus 12.5, 25, or 50 mg/kg betaNF showed a potentiation of Vg synthesis relative to estradiol-only injected fish. These results are significant as they suggest that changing plasma estrogen levels in sexually maturing trout will determine whether or not CYP1A1-inducing compounds may suppress, have no effect, or potentiate estrogen-induced liver Vg synthesis. Depressed Vg synthesis by trout injected with 0.5 mg/kg 17 beta-estradiol plus 50 mg/kg of betaNF correlated with depressed estrogen-binding capacity of liver, as assessed by [3H]17 beta-estradiol binding to liver nuclear protein extracts. Using gel mobility shift assay, the decrease in estrogen responsiveness of liver was not attributed to depressed estrogen response element-estrogen receptor binding. The fish liver vitellogenesis process offers a comparative model with which to further study the mechanism(s) of aryl hydrocarbon receptor-mediated antiestrogenicity and endocrine disruption.

Animals↗
PubMed1985

The effect of estradiol on the sebaceous gland of the hamster ear and its antagonism by tamoxifen.

To evaluate the antagonism between estradiol and tamoxifen in the sebaceous gland of the hamster ear, animals were topically treated, and the size of the sebaceous glands was measured by histoplanimetry. The systemic effects were described by determining the estradiol and testosterone plasma levels and within the testes, and the size of the seminal vesicles and the contralateral sebaceous gland. The administration of 0.1 micrograms estradiol resulted in a diminution in the size of the treated glands but left all other parameters unchanged, indicating a purely local effect. A higher dose of estradiol (1 microgram) further decreased the size of the treated glands, but this was combined with a systemic effect, i.e. low plasma testosterone, decrease in testis size and a diminution of the contralateral ear gland. Ten micrograms of estradiol maximally suppressed all of the androgen effects without side effects. The administration of tamoxifen alone also decreased the size of the sebaceous glands without side effects, but it did not affect the production or effects of androgens. When administered in combination with estradiol, it antagonized the effects of this hormone completely. We conclude that tamoxifen inhibits the negative effect of estradiol on sebaceous-gland size. It acts predominantly in a systemic manner, because a metabolisation to monohydroxytamoxifen is necessary.

Animals↗
PubMed1995

Basal serum follicle stimulating hormone (FSH) and estradiol levels as predictors of pregnancy in unstimulated donor insemination cycles.

PURPOSE: The purpose of this study was to evaluate the utility of basal serum follicle stimulating hormone and estradiol levels in predicting pregnancy in women undergoing artificial insemination with donor sperm for severe male factor infertility. METHOD: A retrospective chart review of 48 women who had at least 2 cycles of artificial insemination with donor sperm and who had undergone testing for basal serum follicle stimulating hormone and estradiol levels prior to or during therapy. RESULTS: There was no difference in age or mean basal serum follicle stimulating hormone between women who conceived (clinical pregnancy) and those who did not. Women who conceived had significantly lower mean serum basal estradiol levels (P = 0.02) and significantly fewer numbers of treatment cycles (P = 0.041). The highest pregnancy rate was among those women with normal basal serum follicle stimulating hormone and estradiol levels. Receiver operating characteristic curve analysis revealed basal serum estradiol to be a more reliable predictor of pregnancy than follicle stimulating hormone. CONCLUSIONS: Basal serum follicle stimulating hormone and estradiol levels may be useful in predicting success with artificial insemination with donor sperm. It may be useful to obtain basal serum follicle stimulating hormone and estradiol prior to initiating artificial insemination with donor sperm.

Adult↗
PubMed1992

Target organ-specific inactivation of drug metabolizing enzymes in kidney of hamsters treated with estradiol.

Chronic treatment of hamsters with estradiol for several months has previously been shown to decrease the specific content of cytochrome P450 in the kidney, a target of hormonal carcinogenesis, but not in liver. The reason for this decrease in metabolic enzyme activity is unknown and has been examined in this investigation. We now report that the decrease in specific content of renal cytochrome P450 by 73% in response to estradiol was not affected by co-treatment with tamoxifen for 1 month. The subcutaneous infusion of 250 micrograms/day estradiol for 7 days lowered renal cytochrome P450 by 71% from control values and was therefore used for further mechanistic studies. This treatment decreased renal activities of estradiol 2- or 4-hydroxylase by 77 to 80%, of 7-ethoxycoumarin-O-deethylase by 66% of control values, respectively, and completely eliminated aryl hydrocarbon hydroxylase activities, whereas liver enzymes remained unaffected. After 7 days of infusion of estradiol, fluorescent products of lipid peroxidation were more than doubled in hamster kidney but remained unchanged in liver. The possibility of enzyme destruction by binding of estradiol 2,3-quinone to metabolizing enzymes was investigated in vitro. In the presence of 2-hydroxyestradiol, cumene hydroperoxide, and microsomes, conditions known to favor the oxidation of the steroid to quinone, the binding of catechol estrogen metabolite to microsomal protein increased 60 fold over control values in the absence of cofactor. Purified rat liver cytochrome P450c also oxidized 2-hydroxyestradiol to 2,3-estradiol quinone. The rate of oxidation was linear for the first 2-3 min, but thereafter decreased with time.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Subcutaneous estradiol pellets for endometrial preparation in donor oocyte recipients with a poor endometrial response.

PURPOSE: The purpose of this study was to evaluate the clinical effectiveness of subcutaneous estradiol pellets in donor oocyte recipients with an inadequate endometrial response. METHODS: The subjects were 13 women with ovarian failure and a maximal endometrial thickness < 10 mm on standard estrogen regimens, as demonstrated during mock and/or prior oocyte donation cycles. They underwent pellet implantation (100-250 mg of estradiol) 6-13 weeks before oocyte donation. RESULTS: maximal (mean +/- SD) endometrial thickness was 8.7 +/- 1.5 mm on standard regimens, in contrast to 11.7 +/- 1.8 mm on pellets, while estradiol levels were 674 +/- 844 and 815 +/- 706 pg/ml, respectively. The estradiol:estrone ratio on pellets was > 1. There was 1 pregnancy with early loss during 10 cycles on other estrogen regimens and 12 pregnancies during 19 cycles on pellets. The pregnancy and implantation rates were, respectively, 63 and 27% on pellets and 41 and 14% on standard regimens in historical controls. CONCLUSIONS: We conclude that estradiol pellets after a single administration provide constant estradiol levels extending into the first trimester of pregnancy, a physiologic estradiol:estrone ratio, and a better endometrial response than standard estrogen regimens. Implantation and pregnancy rates are higher. This approach may be especially suitable for recipients with a poor endometrial response.

Abortion, Spontaneous↗
PubMed2004

Alpha and beta estradiol protect neuronal but not native PC12 cells from paraquat-induced oxidative stress.

Oxidative stress is currently considered a mediator of cell death in several neurodegenerative diseases. Notably, it may play an important role in the degeneration of dopamine neurons of the substantia nigra in Parkinson's disease. We examined the effect of a strong oxidant, the herbicide paraquat, on cell distress using native and neuronal pheochromocytoma PC12 cells. Paraquat administration for 8 hours induced a significant cellular death in both native and in neuronal PC12 cells. Since the anti-oxidant properties of estrogens may promote neuroprotection in vitro and in vivo, we then investigated the ability of estradiol stereoisomers, 17alpha-estradiol and 17- beta-estradiol, to rescue PC12 cells submitted to paraquat-induced oxidative stress. Our results show a protective effect of both estradiol stereoisomers in neuronal PC12 cells treated with paraquat, whereas this effect could not be observed in native PC12 cells. We also demonstrate that estrogen receptor beta protein expression is modulated by paraquat administration in native PC12 cells, while paraquat does not change estrogen receptor beta ?expression in neuronal PC12 cells. Paraquat also decreases estrogen receptor alpha in neuronal PC12 cells, thus suggesting new routes for paraquat to collapse cellular metabolism. Besides, the oxidation of dihydrodhodamine-123 into fluorescent rhodamine in the presence of paraquat but not in presence of paraquat and 17 alpha-estradiol or 17 beta-estradiol, sustain a possible direct scavenging role of both estradiol stereoisomers.

Animals↗
PubMed2001

Antifertility effects of estradiol in adult male rats.

The dose-related effects of estradiol 17-beta at the doses 0.1 pg, 10 microg, 100 microg, 200 microg, 300 microg, 400 microg, 1,000 microg/kg/day were determined on sperm motility, potency, fertility parameters, serum levels of LH, FSH, PRL and testosterone, weights of testes and accessory sex organs, weights of pituitary and adrenal glands. The drug was administered daily via sc route for a period of 60 days. Dose-related effects on fertility parameters of the estradiol-treated male rats were ascertained by allowing them to mate with normal cycling female rats. Estradiol at 0.1 microg/kg/day dose significantly reduced sperm motility with no effects seen on potency or fecundity, serum LH, FSH, PRL or testosterone, weights of testes and accessory sex organs while pituitary weight increased. Estradiol at 10 microg/kg/day dose significantly reduced motility, serum LH, FSH, weights of testes and accessory sex organs, while pituitary weight increased with no effects seen on potency, fecundity, PRL or testosterone. Estradiol at 100-1,000 microg/kg/day dose significantly reduced motility, potency and fecundity, serum LH, FSH and testosterone, weights of testes and accessory sex organs while serum PRL and the weights of pituitary and adrenal glands increased significantly. Histology of the testes revealed disorganization of the cytoarchitecture in the seminiferous tubules, vacuolation, absence of lumen and compartmentalization of spermatogenesis. Estradiol withdrawal, testosterone propionate at 100 pg/kg/day or antiestrogen (tamoxifen citrate) at 400 microg/kg/day prevented the histological changes. It is conduded that estradiol reduces sperm motility even at a low dose. Low doses (<10 microg/kg/ day) appear to maintain whilst high doses (>10 microg/kg/day) reversibly disrupt spermatogenesis. Prevention of disruption by testosterone or antiestrogen indicates crosstalk between androgen and estrogen receptors in Sertoli cells. Loss of potency and fecundity also suggests effects on crosstalk between these receptors in other male reproductive organs.

Animals↗
PubMedDate not supplied

Role of 17-beta-estradiol and progesterone on glucose homeostasis: effects of food restriction (50%) in pregnant and non pregnant rats.

The role of 17-beta-estradiol and progesterone on glucose homeostasis was examined in pregnant and non pregnant rats with or without food restriction (50%). Blood glucose and insulin levels were significantly decreased in food restricted pregnant (PM) compared with control pregnant (PC) and in food restricted non pregnant (M) compared with non pregnant control (C). The plasmatic level of progesterone was similar in PC and PM, while the plasmatic level of 17-beta-estradiol was significantly decreased in PM compared with PC at 15 and 20 days. In spite of food restriction, the changes in the insulin/glucose ratio throughout gestation were similar in PC and PM. A positive and significant relation between 17-beta-estradiol and the level of insulin at day 5 of gestation, and a negative and significant relation between the level of 17-beta-estradiol and level of insulin at day 15 of gestation were found in PC. A negative and significant relation between the levels of progesterone and the levels of insulin at day 5 of gestation, at day 10 this relation is positive and significative, and at day 15 a positive and significant relation exists between levels of 17-beta-estradiol and levels of insulin were found in PM. These results suggest that 17-beta-estradiol acts directly on beta-cells to control insulin secretion. Food restriction does not alter the changes in the sensitivity of tissues to the insulin action, and does modify the action of 17-beta-estradiol and progesterone on beta-cell.

Animals↗
PubMed2000

Radiolabeled estradiol derivatives to predict response to hormonal treatment in breast cancer: a review.

Several radiolabeled steroidal and nonsteroidal estradiol derivatives of which the tumoral uptake is believed to relate quantitatively to the content and binding characteristics of the alpha-estrogen receptor (alphaER) receptor in the target tissue have been synthesized and their imaging potential and clinical usefulness evaluated in vivo in humans. Due to the use of different methodologies and cut-off values for the measurement of alphaER positivity, the use of both quantitative positron emission tomography and semiquantitative single-photon emission tomography, and the difference in patient populations studied, direct comparison of these data is not possible. Individual data, however, fail to substantiate a direct relationship between these radiolabeled estradiol derivatives and alphaER status, in keeping with recent pathophysiological findings demonstrating (1) estradiol sequestration and retention through other than alphaER-mediated, either membrane- or non-membrane-related, mechanisms and (2) an inverse relationship between estradiol uptake and local biosynthesis through aromatization and interconversion in alphaER-positive tumors. Additionally, given the discovery of very high affinity alphaER-like binding sites (Kd, dissociation constant, <0.1 nM), and the potential for underestimation of aER Kd when using ligand binding assays, at least part of the radiolabeled estradiol derivative uptake reflects tumoral perfusion rather than the ligand-receptor binding process. However, the reduction in cellular uptake, membrane sequestration and local biosynthesis of estradiol following tamoxifen treatment in alphaER-responsive tumors should allow early prediction of response to therapy through rapid sequential radiolabeled estradiol scintigraphy with higher accuracy than conventional alphaER estimations, as supported by recent data.

Binding Sites↗
PubMed1980

Estradiol and progesterone receptors in human endometrium: normal and abnormal menstrual cycles and early pregnancy.

Estradiol and progesterone receptor sites (empty or filled with endogenous hormone)have been measured in the cytoplasm and nuclei of human endometrium. Receptor changes have been observed throughout the normal menstrual cycle. During the preovulatory phase the cytoplasmic estradiol receptor sites do not change while the nuclear receptor sites more than double. Cytoplasmic estradiol receptor sites decrease very early in the secretory phase, whereas the decrease in nuclear sites occurs later. Cytoplasmic progesterone receptor sites more than double during the preovulatory phase and show a large decrease immediately after ovulation, when the concentration of nuclear receptor is at its highest. Thus the total cellular concentrations of both estradiol and progesterone receptors are lowest in the late secretory phase. It was found that they are positively correlated with the concentration of plasma estradiol only during the proliferative phase. The concentration of cytoplasmic progesterone receptor is negatively correlated with 17 beta-hydroxysteroid oxidoreductase activity during the secretory phase. In anovulatory cycles the concentrations of estradiol and progesterone receptors are high, similar to those of the late proliferative phase. "luteal insufficiency" is characterized by a very low concentration of estradiol receptor. Early pregnancy endometrium (8 to 10 weeks' gestation) is characterized by a large concentration of progesterone receptor, exceeding those of any period of the menstrual cycle.

Anovulation↗
PubMed1990

Short-term effects of smoking on the pharmacokinetic profiles of micronized estradiol in postmenopausal women.

Because smoking is associated with an increased risk of osteoporosis, yet a decreased risk of endometrial carcinoma, a state of relative hypoestrogenism induced by smoking has been suggested. However, because previous data are unclear and do not reflect current trends in smoking intensity and estrogen prescriptions, we examined the estrogen profiles of postmenopausal women, by smoking status, both before and after oral micronized estradiol. Baseline levels of estrone, estradiol, estrone sulfate, and estrone glucuronide were similar in nonsmokers and smokers, but unbound (non-sex-hormone-binding-globulin--bound) estradiol was significantly lower in smoking women (p less than 0.05) and sex-hormone-binding-globulin--binding capacity was higher (p less than 0.001). After 1 or 2 mg of micronized estradiol, estrone and estradiol serum profiles were similar but unbound estradiol was significantly lower in women who were smokers (p less than 0.05). Serum estrone glucuronide rose with treatment but was indistinguishable in nonsmokers and smokers. However, maximum changes in serum estrone sulfate were greater in smokers after administration of estrogen, suggesting a hepatic effect. Urinary estrone glucuronide levels increased after 8 hours of oral estrogen but were similar in nonsmokers and smokers with the two doses. It appears that even moderate smoking, as studied here, induces significant changes in hepatic estrogen metabolism and is best reflected by alterations in serum estrone sulfate and sex-hormone-binding-globulin--binding capacity that result in decreased serum unbound estradiol. However, these changes do not appear to require increasing the estrogen dosage to achieve physiologic levels of estrogen in postmenopausal smokers.

Estradiol↗
PubMed1994

Acute effects of 17 beta-estradiol on the rat heart.

OBJECTIVE: Our purpose was to study the acute effects of 17 beta-estradiol on mechanical and electrical activities of cardiac function and on coronary arteries in the rat heart. STUDY DESIGN: The effects of 17 beta-estradiol were studied on perfused working heart isolated from Charles River male rats. Heart rates, coronary flow, aortic flow, and left ventricular pressure were measured. To avoid coronary interaction, chronotropic and inotropic effects were also tested on isolated atria. Data were analyzed with the paired Student t test. RESULTS: 17 beta-Estradiol produced a dose-dependent negative chronotropic effect in right atria but did not affect the contractility of left atria. A decrease in heart rate was also observed in perfused hearts treated with 5 x 10(-6) mol/L 17 beta-estradiol. 17 beta-Estradiol (5 x 10(-6) mol/L) significantly increased coronary flow (p < 0.005) but had a negligible effect on cardiodynamic index values. A significant effect of 17 beta-estradiol on cardiac function was observed when coronary arteries were precontracted with acetylcholine. CONCLUSION: Both the experimental coronary vasodilatory effect and the negative chronotropic effect of 17 beta-estradiol support the clinical observations that suggest that this hormone may have an important role in prevention of cardiovascular diseases.

Acetylcholine↗
PubMed1994

Human preterm birth is associated with systemic and local changes in progesterone/17 beta-estradiol ratios.

OBJECTIVE: The purpose of this study was to determine whether human preterm birth is associated with changes in 17 beta-estradiol and progesterone concentrations in maternal plasma and amniotic fluid. STUDY DESIGN: Forty healthy women in preterm labor with singleton pregnancies and intact membranes at 32 to 36 weeks of gestation who underwent amniocentesis for evaluation of the microbiologic status of the amniotic cavity were classified into the following two groups: 20 women who were delivered within 1 week from the amniocentesis (preterm delivery group) and 20 who were delivered at term (term delivery group). Maternal plasma and amniotic fluid concentrations of progesterone and 17 beta-estradiol were measured with sensitive and specific commercially available radioimmunoassay kits. RESULTS: The median amniotic fluid concentration of 17 beta-estradiol was significantly higher in women delivered prematurely than in those who were delivered at term (1.5 ng/ml vs 0.9 ng/ml, p = 0.0001). Moreover, the median plasma 17 beta-estradiol concentration was also significantly higher in the preterm delivery group than in the term group (14.1 ng/ml vs 6.9 ng/ml, p = 0.022). In contrast, no significant difference was found in amniotic fluid and plasma concentrations of progesterone between these two groups (24.5 ng/ml vs 27.5 ng/ml and 132.0 ng/ml vs 107.5 ng/ml, respectively). The median amniotic fluid progesterone/17 beta-estradiol ratio was significantly lower in the preterm delivery group than in those delivered at term (18.4 vs 33.6, respectively, p = 0.0017). Moreover, the median plasma progesterone/17 beta-estradiol ratio was also significantly lower in the preterm delivery group than in the term group (9.8 vs 17.0, respectively, p = 0.016). CONCLUSION: Human preterm birth is associated with significantly lower progesterone/17 beta-estradiol ratios than those of women with preterm labor delivered at term.

Adult↗
PubMed1985

Induction of a decrease in renal NAD+-dependent 15-hydroxyprostaglandin dehydrogenase activity by estradiol in rats.

The effect of estradiol administration on renal and pulmonary NAD+-dependent 15-hydroxyprostaglandin dehydrogenase activities in rats was studied. Estradiol induced a significant decrease in renal but not in pulmonary enzyme activity. Kinetic parameters for the renal enzyme from control and treated groups were compared. An identical apparent Km for prostaglandin E2 was obtained for the enzyme from both groups. Vmax in the treated group was progressively decreased and plateaued 1 day after estradiol injection. The estradiol-induced decrease in renal enzyme activity was blocked by an anti-estrogen, nafoxidine, suggesting that the effect of estradiol was a was a receptor-mediated event. The decrease in renal prostaglandin catabolic enzyme activity induced by estradiol may result in prolonging the half-life of circulating prostacyclin and may account, in part, for the anti-thrombogenic effect of estradiol.

Animals↗
PubMed1978

Chromatin binding of estradiol in the hypothalamus and cortex of male and female rats.

Gonadal steroids are thought to act by activation of the genome following cytoplasmic binding, translocation of the hormone--receptor complex to the nucleus and chromatin binding at specific acceptor sites. This study examined the kinetics of chromatin binding of estradiol by hypothalamic and cortical cells of adult gonadectomized male and female rats. In both sexes binding was found to be limited to hypothalamic cells. The kinetics of binding differed between the sexes, estradiol being retained less well in males. In females hypothalamic chromatin binding was shown to be of limited capacity and to be competitively inhibited by unlabeled estradiol. Unlabeled testosterone inhibited estradiol binding when administered subcutaneously 3 h before the estradiol, but not by testosterone when administered either intravenously or concurrently with the estradiol. It was suggested that the observed sex difference in hypothalamic chromatin binding might underlie the relative insensitivity of the male to the lordosis-inducing properties of estradiol.

Animals↗
PubMed1985

Estradiol benzoate decreases nigral GABAergic activity in male rats.

Repeated doses of estradiol benzoate (10 micrograms/kg, s.c., once a day for 2, 5 or 8 days) to male rats decreased gamma-aminobutyric acid (GABA) content and glutamate decarboxylase (GAD) activity in substantia nigra (SN) but failed to change these parameters in hippocampus, cerebral cortex, cerebellum, lateral septum and olfactory tubercle. In the caudate nucleus, estradiol benzoate decreased GABA concentration but did not modify GAD activity. A decrease in nigral GABA concentration and GAD activity was also observed 24 and 48 but not 3 h after a single injection of estradiol benzoate. These data are consistent with results on GAD activity reported by McGinnis et al. in ovariectomized rats. Kinetic analysis of nigral GAD activity revealed that repeated estradiol benzoate injection reduced the Vmax without affecting the Km of GAD. Estradiol benzoate also reduced the rate of nigral GABA accumulation resulting from local infusion of gabaculine, suggesting that the steroid decreases GABA turnover in male rat SN. Hypophysectomy decreased GABA content and GAD activity in SN and GABA content in striatum. Administration of estradiol benzoate for 8 days to hypophysectomized rats failed to decrease further these parameters. Taken together, these data suggest that estradiol benzoate decreases SN GABAergic activity and that the integrity of the pituitary gland is required for this effect.

Animals↗
PubMed1991

A site for estradiol priming of progesterone-facilitated sexual receptivity in the ventrolateral hypothalamus of female guinea pigs.

The induction of progestin receptors by estradiol in the mediobasal hypothalamus (MBH) has been correlated with progesterone facilitation of sexual receptivity in female guinea pigs. We used an immunocytochemical technique to visualize the induction of progestin receptors by estradiol in a population of neurons correlated with estradiol-induced responsiveness to progesterone. Progestin receptor-immunoreactivity (PR-IR) and responsiveness to progesterone-facilitation of sexual behavior were induced by intracranial implantation of small bilateral cannulae (28- or 33-gauge) containing 1 or 10% estradiol diluted with cholesterol. In the first experiment, 28-gauge cannulae containing estradiol were effective only when implanted in the rostral part of the MBH. In the second experiment in which 33-gauge cannulae were used, behavioral responsiveness to progesterone was induced only when the cannulae were localized bilaterally in the rostro-ventral part of the ventrolateral hypothalamus (VLH). The presence of estradiol-induced PR-IR within the rostro-ventral VLH was correlated with the ability of progesterone to facilitate sexual behavior. These data suggest that neurons containing estrogen-induced progestin receptors specifically within the rostro-ventral VLH are involved in progesterone facilitation of sexual receptivity in estradiol-primed guinea pigs.

Animals↗