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PubMed1987

The effect of percutaneous estradiol and natural progesterone on postmenopausal bone loss.

The effect of percutaneous estradiol alone and combined with natural progesterone on postmenopausal bone loss was studied. A total of 57 women who had experienced a natural menopause 6 months to 3 years previously entered the study. After an initial examination the women were allocated in a blinded pattern to treatment with 3 mg of percutaneous estradiol or placebo. The code was broken after 1 year of treatment, and the women receiving estradiol continued with a cyclic addition of progesterone, whereas those receiving placebo continued with placebo. The women were examined every 3 months during the 2 years of treatment. Measurement of the bone mineral content in the forearms (single photon absorptiometry) and the spine and total skeleton (dual photon absorptiometry) showed a significant decrease of 5% to 7% in the placebo group during the 2 years of treatment, whereas it remained constant in all bone compartments in the estradiol group. Addition of progesterone did not influence the results. Biochemical estimates of calcium metabolism changed toward a premenopausal level in the estradiol group but remained unchanged in the placebo group. We conclude that percutaneous estradiol is effective as preventive therapy of postmenopausal bone loss and that addition of progesterone does not influence bone or calcium metabolism.

Administration, Cutaneous↗
PubMed1988

A randomized comparison of nonoral estradiol delivery in postmenopausal women.

We compared the transdermal and subdermal routes of estrogen administration with respect to the constancy of estrogen delivery and metabolic effects. Twenty postmenopausal women were randomized to receive either two 25 mg estradiol pellets subdermally (n = 10) or a 0.1 mg estradiol transdermal patch twice weekly (n = 10). Blood was sampled at 0, 2, 4, 6, 8, 12, 24, and 72 hours and 1, 2, 4, 8, 12, 16, 20, and 24 weeks (fasting samples at 0, 12, and 24 weeks), and a fasting urine was obtained after diuresis at 0, 12, and 24 weeks. In a 72-hour profile, serum estradiol levels (mean +/- SE) were highest at 24 hours (179 +/- 20 pg/ml) and fell to 139 +/- 16 pg/ml at 72 hours in the pellet group. In the patch group, estradiol levels rose rapidly to 152 +/- 33 pg/ml at 4 hours, remained relatively constant over 8 hours, and fell to 46 +/- 10 pg/ml at 72 hours. At 1 week, estradiol levels in the pellet group were 113 +/- 12 pg/ml and remained relatively constant for 24 weeks. In contrast, estradiol levels in the patch group were 52 +/- 11 pg/ml at 1 week and then varied widely until 24 weeks, when the levels were 89 +/- 26 pg/ml. The mean estradiol/estrone ratio ranged between 1 and 2.5 in both groups but fluctuated widely in the patch group. Follicle-stimulating hormone was suppressed in both groups; however, the decrement in the pellet group was greater (p less than 0.002). There was a significant increase in high-density lipoprotein cholesterol and a decrease in total cholesterol/high-density lipoprotein cholesterol at 12 weeks with the pellet but only at 24 weeks with the patch. The urinary calcium/creatinine ratio was reduced more consistently with the pellet than with the patch. Hot flushes were eliminated in all subjects.

Administration, Cutaneous↗
PubMed1991

Forward shift in the initiation of the nocturnal estradiol surge in the pregnant baboon: is this the genesis of labor?

Daily (9 AM and 6 PM) blood samples were obtained from the inferior vena cava during the last trimester of pregnancy in a tethered baboon model. In addition, three 24-hour (hourly blood sampling) studies were performed at days 143 to 147, 158 to 162, and 172 to 177 of pregnancy. Dramatic 24-hour rhythms in progesterone and estradiol were detected, with both steroids surging nocturnally. Early in the third trimester the estradiol surge followed the progesterone surge. However, approximately 10 to 12 days before delivery, the initiation of the nocturnal estradiol surge shifted forward, thus preceding the progesterone surge. This forward shift in the estradiol surge created a daily (3 to 5 hours) window of elevated estradiol-to-progesterone ratio and appears to coincide with the initiation of nocturnal uterine contractions. The nocturnal uterine contractions can be inhibited by an oxytocin antagonist. We hypothesize that this forward shift in the initiation of the estradiol surge induces nocturnal uterine contractions by oxytocin release and/or increase in uterine oxytocin receptors and generates molecular messages that are the genesis for labor and delivery in the baboon.

Animals↗
PubMed1992

Culture characteristics of human endometrial glandular epithelium throughout the menstrual cycle: modulation of deoxyribonucleic acid synthesis by 17 beta-estradiol and medroxyprogesterone acetate.

OBJECTIVE: The purpose of this study was to evaluate the culture characteristics and cell proliferation of human endometrial glandular epithelial cells in primary culture on extracellular matrix and to evaluate sex steroid modulation of this process. STUDY DESIGN: We examined the culture characteristics in 53 endometrial gland preparations obtained throughout the menstrual cycle and determined the incorporation of tritiated thymidine in endometrial epithelial cells as a measure of deoxyribonucleic acid synthesis (cell proliferation) in the presence and absence of 17 beta-estradiol and medroxyprogesterone acetate. RESULTS: Good culture maintenance of endometrial epithelial monolayers on extracellular matrix was observed from glands derived from proliferate phase endometrium (21 of 23), whereas poor adherence and culture maintenance was observed in all 30 of specimens from the secretory phase. With 17 beta-estradiol treatment for 22 hours, tritiated thymidine incorporation was not different from control, but medroxyprogesterone acetate treatment for 22 hours was associated with diminished tritiated thymidine incorporation by 36% (p < 0.004). When 17 beta-estradiol (10(-8) mol/L) was included in the incubation medium from the time of initial culture, tritiated thymidine incorporation on day 4 was 40% of control (p < 0.006), and tritiated thymidine was not suppressed further by 22 hours of treatment with medroxyprogesterone acetate (10(-7) mol/L). In spite of cellular spread of endometrial epithelial cells to subconfluence, deoxyribonucleic acid content per well did not increase over time in culture. CONCLUSIONS: We conclude that exposure of endometrial glands to progesterone in vivo inhibits adherence and the establishment of cell monolayers cultured on a thin layer of extracellular matrix. Because 17 beta-estradiol treatment in culture for 22 hours does not increase tritiated thymidine incorporation, it is possible that 17 beta-estradiol exerts its proliferative effect on the endometrial epithelium by an indirect action mediated by stromal cells. The effects of 17 beta-estradiol and medroxyprogesterone acetate on deoxyribonucleic acid synthesis in endometrial epithelial cells may represent an action on a stem cell population of dividing cells or a terminally differentiated cell population that undergoes programmed cell death.

Cells, Cultured↗
PubMed1995

Sustained-release estradiol implants and a levonorgestrel-releasing intrauterine device in hormone replacement therapy.

OBJECTIVE: Efficacy and acceptability of continuous combined parenteral hormone replacement consisting of subdermal estradiol delivery and intrauterine progestin delivery was studied. STUDY DESIGN: Thirty-six volunteer postmenopausal women seeking treatment for climacteric symptoms participated in this open, randomized study. The subjects received either one or three subdermal implants with a controlled daily release of estradiol in vitro. Progestin therapy was carried out with a levonorgestrel-releasing intrauterine device. Climacteric symptoms and serum concentrations of estrone, estradiol, follicle-stimulating hormone, and sex hormone-binding globulin were followed up for 1 year. The subjects kept daily records of bleeding. RESULTS: Serum estradiol concentrations with the set of three implants were stable during the follow-up period; the range of mean serum estradiol concentrations was 45 to 57 pg/ml. Four women, all from the group with one implant, discontinued the study after 6 months because of the return of climacteric symptoms. In spite of different daily estradiol doses, the patterns of bleeding were similar in both groups. At the end of the follow-up year 72% of the women had had no bleeding or spotting in the previous 3 months. CONCLUSION: Our results suggest that by combining subdermal and intrauterine steroid delivery systems postmenopausal hormone replacement therapy can be carried out successfully without daily effort and with minimal or no bleeding.

Drug Implants↗
PubMed1992

Estradiol regulates class I alcohol dehydrogenase gene expression in renal medulla of male rats by a post-transcriptional mechanism.

Rat kidney contains alcohol dehydrogenase (ADH) activity which appears to be identical to the class I ADH expressed in liver. Treatment of male rats with estradiol for 10 days induced ADH activity and protein in the kidney approximately 3-fold. This was not the result of suppression of testosterone levels by estrogen, as castration did not increase ADH activity. In situ hybridization of kidney sections showed that ADH transcripts were localized to the medulla, that the basal level of mRNA is very low in the male, and that the induction of ADH mRNA by estradiol was approximately 10-fold. As estimated from Northern blot analysis, the induction of the mRNA was approximately 7-fold. Thus, induction of ADH mRNA substantially exceeded the increase of ADH activity and protein. Since the estradiol-treated rats lost weight relative to the oil-injected controls, the effect of starvation on ADH mRNA in kidney was examined. Starvation decreased kidney ADH activity by about 30% but increased mRNA about 2-fold. Time course experiments demonstrated induction of ADH mRNA by estradiol within 1 h with the maximum level achieved by 24 h. The transcription rate of the ADH gene as assessed by nuclear run-on assays performed at 1 and 24 h after treatment with estradiol was unchanged. We conclude that estradiol induces ADH mRNA in kidney by a post-transcriptional mechanism.

Alcohol Dehydrogenase↗
PubMed1981

Alterations of plasma HDL lipids and apolipoproteins in female rats treated with ethynyl estradiol.

Female Sprague-Dawley rats (160-200 g body weight) were injected subcutaneously daily for 14 days with 1, 5, 15, 50 or 100 micrograms ethynyl estradiol in sesame oil/kg body weight, or with oil alone. Food consumption was restricted to 15 g/day, and animals were fasted overnight before exsanguination. Concentrations of plasma cholesteryl ester decreased with increasing dosage of ethynyl estradiol, as a result of decreases in HDL cholesteryl ester. Concentrations of plasma unesterified cholesterol were not altered by treatment; the tendency for a decrement in the HDL cholesterol was not statistically significant. Plasma and HDL phospholipid also tended to decrease with increasing dose of ethynyl estradiol. Plasma levels of apolipoprotein A-I increased on treatment with 5 micrograms ethynyl estradiol/kg but were diminished at a dose of 50 micrograms ethynyl estradiol/kg. The ultracentrifugally isolated high density lipoproteins were delipidated and the distribution of apolipoproteins was characterized by SDS-polyacrylamide gel electrophoresis and esoelectric focusing. The proportion of apolipoprotein E in HDL was depressed, while apolipoprotein A-I was increased and apolipoprotein C unchanged by treatment with ethynyl estradiol. Clearly, the alterations in plasma HDL lipid levels resulting from treatment with ethynyl estradiol were accompanied by distinct changes in composition of the apolipoproteins of HDL, and a biphasic response dependent on dose of the drug. A possible mechanism for the diminution in the proportion of HDL apolipoprotein E may be the enhanced removal of the apolipoprotein E-rich (HDL1) subfraction of the HDL from the circulation on treatment with ethynyl estradiol.

Animals↗
PubMed1991

Estradiol increases the secretion of hepatic lipase by rat hepatocyte cultures.

Hepatic lipase (EC 3.1.1.3) is synthesized and secreted by parenchymal hepatocytes and binds to endothelial cells of liver sinusoids. The present study shows that the activity of hepatic lipase secreted by hepatocyte cultures from male rats in increased approx. 6-fold after 10 h culture with 10 microM 17 beta-estradiol. The stimulatory effect of 17 beta-estradiol is biphasic and declines at higher concentrations. In hepatocytes from male rats: progesterone, unlike 17 beta-estradiol, had only a small stimulatory effect when present as the sole hormone and a small inhibitory effect in the presence of 17 beta-estradiol, while testosterone and dexamethasone had no effect. Hepatocyte cultures from female rats had a higher basal rate of hepatic lipase secretion than cells from male rats and showed a smaller stimulation by 17 beta-estradiol. These results suggest that 17 beta-estradiol might regulate the secretion of hepatic lipase by hepatocytes, and presumably the activity of the enzyme at either the endothelial surface of the liver sinusoids or at extrahepatic sites.

Animals↗
PubMed1991

Effect of 17 beta-estradiol on PAF and prostaglandin levels in oophorectomized rat uterus.

The effects of 17 beta-estradiol on the levels of platelet-activating factor (PAF) and prostaglandins and their precursor phospholipid in the uterus of oophorectomized rats were studied. Oophorectomy results in the decrease in the uterine PAF level to one-third of that in natural estrus. This level was recovered by subcutaneous administration of 17 beta-estradiol. The level of uterine phospholipids, which are rich in arachidonic acid, was significantly decreased by estradiol treatment. More arachidonate-PC was depleted than arachidonate-PE. The molecular structure was confirmed by gas chromatography-mass spectrometry. The amount of PGF2 alpha in the oophorectomized uterine tissue was 10-times that of PAF, but like the latter, increased 3-4 times on estradiol treatment. The chemical structures of PAF and PGF2 alpha formed on estradiol treatment were confirmed by mass spectrometry. The present data strongly suggest a correlation between the formations of PAF and PGF2 alpha, and indicate that estradiol may regulate the physiological formations of PAF and PGs in non-pregnant rat uterus.

Animals↗
PubMed1985

Interaction of estradiol and high density lipoproteins on proliferation of the human breast cancer cell line MCF-7 adapted to grow in serum free conditions.

The responsiveness of the human mammary carcinoma cell line MCF-7 to estradiol and tamoxifen treatment has been studied in different culture conditions. Cells from exponentially growing cultures were compared with cells in their initial cycles after replating from confluent cultures ("confluent-log" cells). It has been observed that estradiol stimulation of tritiated thymidine incorporation decreases with cell density and that "confluent-log" cells are estrogen unresponsive for a period of four cell cycles in serum-free medium conditions. On the other hand, growth of cells replated from exponentially growing, as well as from confluent cultures, can be inhibited by tamoxifen or a combined treatment with tamoxifen and the progestin levonorgestrel. This growth inhibitory effect can be rescued by estradiol when cells are replated from exponentially growing cultures. The growth inhibitory effect cannot be rescued by estradiol alone (10(-10) to 10(-8) M) when cells are replated from confluent cultures. In this condition, the addition of steroid depleted serum is necessary to reverse the state of estradiol unresponsiveness. Serum can be replaced by high density lipoproteins but not by low density lipoproteins or lipoprotein deficient serum. The present data show that estradiol and HDL interact in the control of MCF-7 cell proliferation.

Breast Neoplasms↗
PubMed1988

Stimulation of cadmium uptake by estradiol in the kidney of male rats treated with cadmium.

The present study was carried out to analyze the sex differences in the retention of Cd in rats treated with a small amount of Cd, and its mechanisms. Cd and Zn concentrations in the kidney and liver of female rats treated with 28 nmol Cd or 1 nmole Zn were significantly higher than those in male rats. Pretreatment with estradiol (1.8 mumol/kg of b.w., twice a day, 6 consecutive days) increased the Cd and Zn concentrations in the kidney of male rats treated with Cd or Zn. Incubation of MDCK cells with 10(-5) M estradiol, 10(-5) M stilboestrol and 10(-5) M progesterone caused a significant increase in Cd uptake. These results suggest that endogenous female sex hormones may play a role in a higher concentration of Cd and Zn in the kidney of female rats than that in male rats. The basal level of metallothionein (MT) in the liver and kidney of control female rats was within the same range as that in the control male rats. Cd and Zn accumulations caused by pretreatment with estradiol in the kidney of male rats treated with Cd or Zn were so low (Cd: 38 ppb, Zn: 1.0 ppb) as to be probably unable to induce the synthesis of MT. An increase in the concentration of Cd in the cultured renal cells occurred 1 hr after treatment with estradiol and Cd. Pretreatment with estradiol alone also resulted in a modification of the concentration of Na and K, which cannot be bound to MT. Together, all of the above findings suggest that estradiol directly increases the accumulation of Cd into the renal cells without inducing the synthesis of MT.

Animals↗
PubMed1988

Effects of the antiestrogen LY 117018 on the modulation by ethinyl estradiol of the metabolism of [1-14C]oleic acid by perfused livers from normal and ovariectomized rats.

Intact female Sprague-Dawley rats (195-249 g) and rats that had been ovariectomized (210-285 g) were injected subcutaneously for 14 days with ethinyl estradiol (15 micrograms/kg), the antiestrogen LY 117018 (500 micrograms/kg), both drugs simultaneously, or the vehicle (sesame oil) alone. Livers were removed and perfused in vitro in a recycling system. The administration of LY 117018 alone did not affect the secretion of triacylglycerol by livers from normal rats but decreased the secretion of triacylglycerol by livers from ovariectomized rats. When the drugs were administered concurrently to either normal or ovariectomized animals, the increase in the concentration of triacylglycerol and the decrease in the concentration of cholesteryl esters in the plasma produced by ethinyl estradiol were prevented. When administered to either intact or ovariectomized rats, ethinyl estradiol alone stimulated the synthesis and secretion of triacylglycerol and cholesteryl esters by perfused livers isolated from these animals. The simultaneous administration of LY 117018 with ethinyl estradiol prevented this stimulation of the hepatic synthesis and secretion of triacylglycerol and cholesteryl esters. The depression of ketogenesis observed with livers from rats administered ethinyl estradiol alone was reversed by concurrent administration of LY 117018. The concurrent administration of the estrogen and antiestrogen did not result, however, in a complete blockade of the estrogen-induced elevation of hepatic triacylglycerol synthesis and depression of ketogenesis. The incorporation of [1-14C]oleic acid into the triacylglycerol and ketone bodies by livers from ovariectomized rats was less than that of livers from normal rats. It is clear that the antiestrogen antagonizes the actions of ethinyl estradiol on hepatic lipid metabolism. Furthermore, the use of the antiestrogen LY 117018 in these experiments allows the probable conclusion that the modulation of hepatic metabolism of fatty acid by estrogen is mediated by conventional estrogenic receptors.

Animals↗
PubMed1993

Modulation by estradiol and progesterone of the GTP effect on striatal D-2 dopamine receptors.

Agonist binding properties of rat striatal D-2 dopamine (DA) receptors were investigated after in vivo or in vitro estradiol or progesterone exposures in order to elucidate the mechanism of action of steroid hormones on DA receptors. Chronic estradiol treatment of ovariectomized rats (10 micrograms, twice each day, for 2 weeks) increased lateral striatum total receptor density and left unchanged the proportion and affinity of the agonist high- and low-affinity states of this receptor in the striatum. In addition, when GTP was added in DA competition for [3H]spiperone binding experiments, D-2 receptors in the medial part of the striatum from estrogen-treated animals were more sensitive to GTP than those in the lateral part, whereas GTP had equal activity in both parts of the striatum in vehicle-treated rats. With apomorphine, but not with DA competition for [3H]spiperone binding, addition of estradiol (1 nM) to striatal homogenates of intact male rats prevented the expected shift of the high- to the low-affinity state of D-2 receptors, normally induced by GTP (100 microM) under these conditions. This effect of estradiol was not observed in the presence of 4 mM MgCl2, while in vitro progesterone (100 nM) had no effect in either the absence or presence of MgCl2. In addition, in vivo chronic progesterone treatment of ovariectomized rats left striatal [3H]spiperone density and affinity unchanged. Moreover, 1 nM estradiol increased the IC50 of GTP for inhibition of [3H]N-propylnorapomorphine binding to the high-affinity state of striatal D-2 receptors. This effect was also observed but decreased by 2-fold in the presence of MgCl2. Our data suggest that estradiol in vivo and in vitro interferes with the effect of GTP on striatal D-2 DA receptors.

Animals↗
PubMed1984

Effects of estradiol and prolactin on incertohypothalamic dopaminergic neurons in the male rat.

The activity of incertohypothalamic, tuberoinfundibular, mesolimbic and nigrostriatal dopamine (DA) neurons was estimated by measuring the rate of turnover of DA (decline of DA after alpha-methyltyrosine) in brain regions containing the cell bodies and terminals of these neurons. Estradiol benzoate (25 micrograms/kg/day X 3; s.c.), markedly increased the concentration of prolactin in plasma and increased the rate of turnover of DA in median eminence, but failed to alter DA neuronal activity in the striatum or nucleus accumbens. An intracerebroventricular injection of prolactin (10 micrograms/rat, 12 h) mimicked the effect of estradiol on the turnover of DA in the median an eminence. Within the incertohypothalamic DA system, both estradiol and prolactin increased DA turnover in the dorsomedial nucleus but decreased DA turnover in the rostral periventricular, medial preoptic and preoptico-suprachiasmatic nuclei. Hypophysectomy decreased the tonic activity of tuberoinfundibular DA neurons, but failed to alter the activity of incertohypothalamic DA neurons. The stimulatory effects of estrogen on DA turnover in the median eminence and dorsomedial nucleus, and the inhibitory effects of this hormone on rostral hypothalamus DA neurons were blocked by hypophysectomy. Taken together these results suggest that estradiol induced changes in intact male rats are mediated by prolactin. Estradiol increased incertohypothalamic DA neuronal activity in the medial preoptic and preoptic-suprachiasmatic nuclei of hypophysectomized rats suggesting that in the absence of circulating prolactin, estradiol has a direct stimulatory effect on incertohypothalamic DA neurons in the rostral, periventricular hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Intracranial estradiol in ovariectomized guinea pigs: effects on ingestive behaviors and body weight.

The present study was undertaken to evaluate the effects of intracranial estradiol stimulation on food intake (FI), water intake (WI), and body weight (BWt) of ovariectomized guinea pigs (GPs). Thirty-five GPs were implanted with bilateral guide cannulae aimed at either the ventromedial hypothalamus, paraventricular nucleus (PVN), or preoptic area and then were stimulated unilaterally with cholesterol and estradiol 17-beta, yielding a total of 70 stimulation sites. Across all GPs, estradiol implants significantly reduced FI, WI and BWt relative to implants of cholesterol. The possibility that the behavioral changes observed were due to the peripheral rather than central effects of the implants was evaluated by comparing the results of stimulations which produced vaginal membrane rupture (VMR) to the results of cases without VMR. There were no significant differences between these groups on any of the dependent variables studied, indicating that peripheral estradiol sufficient to induce VMR was neither necessary nor sufficient to account for the behavioral changes. Histological analysis revealed that implants in the ventromedial-arcuate region (VM/ARC) and PVN significantly lowered FI and BWt, with the effects being greatest in the PVN. Placements in other areas, on the average, did not significantly suppress FI or BWt. The effect of central estradiol on WI was more diffuse. No significant effect of implant location was found for the estrogenic suppression of drinking. These findings are the first demonstration that estradiol applied to particular brain areas can lower FI, WI, and BWt of ovariectomized GPs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Estradiol induces rapid remodelling of plasma membranes in developing rat cerebrocortical neurons in culture.

Exo-endocytotic images and intramembrane particles were quantitatively assessed in freeze-fracture replicas from the plasma membrane of dispersed fetal rat cortical neurons (day 16 gestation) grown for 24 days in culture. The addition of 10(-10) M 17 beta-estradiol to the culture medium resulted in a significant increase in the numerical density of exo-endocytotic images within 1 min. A further increase of the number of exo-endocytotic images associated to a significant decrease in the number of intramembrane particles was observed in cells exposed for 10 min to 17 beta-estradiol. Similar results were observed when the cells were exposed to 17 beta-estradiol for 17 days. No effects on exo-endocytotic images and intramembrane particles were observed when 17 alpha-estradiol was added, instead of 17 beta-estradiol, to the cultures. These results indicate that physiological levels of 17 beta-estradiol can have rapid effects upon the ultrastructure of the neuronal membrane of developing cerebrocortical neurons.

Animals↗
PubMed1992

Effects of PVN lesions on the responsiveness of female rats to estradiol.

Previous research has shown that the paraventricular nucleus of the hypothalamus (PVN) is an important site of action for the effects of estradiol on feeding behavior. The recent finding that estrogenic stimulation of the PVN lowers food intake without inducing lordosis suggests that the effects of estradiol on feeding and sexual behaviors are organized separately within the brain. Whether the effects of estradiol on food intake can be attenuated by PVN lesions is therefore a question of practical and theoretical interest. In this experiment we examined the behavioral responsiveness of females with PVN lesions to peripheral treatment with estradiol. 32 adult, female rats received either bilateral or sham lesions of the PVN. All subjects were ovariectomized 2 weeks after the lesion. 2 Weeks following ovariectomy, half of the animals were injected with 2 micrograms of estradiol benzoate (EB) for 3 days, and half were injected with the oil vehicle. 10 days later, the treatment conditions for each subject (oil or EB) were reversed. Histological analysis indicated that 9 females had bilateral lesions of the PVN and 4 had bilateral lesions of the dorsomedial nucleus of the hypothalamus (DMN); 11 animals received sham lesions. Compared with oil treatment, EB injections significantly lowered water intake and body weight gain in all groups. However, food intake was suppressed in the DMN and sham but not in PVN-lesioned females. In addition, statistical analyses indicated that EB treatment induced similar levels of female sexual behavior in all groups. Thus, PVN lesions did not interfere with the ability of estradiol to stimulate lordosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

The role of estradiol and progesterone in phased synaptic remodelling of the rat arcuate nucleus.

During the estrous cycle there is a phasic synaptic remodelling in the hypothalamic arcuate nucleus, consisting in a loss and regain of axo-somatic synapses during the 48 h period between the morning of proestrus and the morning of metestrus. Synaptic changes are accompanied by cyclic modifications in the number of intramembrane particles in the plasma membrane of arcuate neuronal somas. To test the effect of the ovarian steroids on arcuate axo-somatic synapses we treated castrated females either with oil vehicle, 17 beta-estradiol, progesterone, or a combination of estradiol and progesterone, and observed them for 48 h. The number of axo-somatic synaptic profiles showed a 33% fall by 24 h after estradiol treatment and returned to control levels by 48 h. The effect of estradiol on axo-somatic synapses was accompanied by a marked and reversible modification of the number of intramembrane particles in the plasma membrane of arcuate neuronal somas. Progesterone alone did not affect the number of axo-somatic synaptic profiles nor the number of intramembrane particles, but when administered together with estradiol, blocked the effects of estradiol on neuronal membrane and synapses.

Animals↗