scholarly journals Temporal expression of estrogen receptor α in the hypothalamus and medulla oblongata during fasting: a role of noradrenergic neurons

2006 ◽  
Vol 190 (3) ◽  
pp. 593-600 ◽  
Author(s):  
Beverly A S Reyes ◽  
Hiroko Tsukamura ◽  
Helen I’Anson ◽  
Maria Amelita C Estacio ◽  
Kanjun Hirunagi ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Brain Regions ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Noradrenergic Neurons ◽  
Anatomical Relationship ◽  
Relationship Of ◽  
Lh Secretion

Fasting-induced LH suppression is augmented by estrogen in female rats. We investigated the temporal changes in the number of estrogen receptor α (ERα)-immunoreactive (ir) cells in various brain regions in ovariectomized rats fasted for 6, 24, 30, and 48 h, commencing at 1300 h. We also determined the anatomical relationship of ERα immunoreactivity and dopamine-β-hydroxylase (DBH) neurons in the A2 region of the nucleus of the solitary tract (NTS) and the paraventricular nucleus (PVN). The number of ERα-ir cells significantly increased after 30 h from the onset of fasting in the PVN and NTS compared with the unfasted controls and was sustained until 48 h. In the A2 region of 48-h fasted rats, 46.75% DBH-ir cells expressed ERα, and this was significantly higher than in unfasted controls (8.16% DBH-ir cells expressed ERα). In the PVN, most ERα-ir neurons were juxtaposed with DBH-ir varicosities. These results suggest that ERα is expressed in specific brain regions at a defined time from the onset of fasting. In addition, the anatomical relationship of noradrenergic and ERα-ir neurons in the A2 region and PVN may suggest a role for estrogen in increasing the activity of noradrenergic neurons in the A2 region and enhancing sensitivity of the PVN to noradrenergic input arising from the lower brainstem and thereby augmenting the suppression of LH secretion during fasting.

scholarly journals The Role of the Medial and Central Amygdala in Stress-Induced Suppression of Pulsatile LH Secretion in Female Rats

Endocrinology ◽  
2011 ◽  
Vol 152 (2) ◽  
pp. 545-555 ◽  
Author(s):  
Yuanshao Lin ◽  
Xiaofeng Li ◽  
Micol Lupi ◽  
James S. Kinsey-Jones ◽  
Bei Shao ◽  
...  
Keyword(s):  
Pulse Generator ◽  
Reproductive Function ◽  
Ibotenic Acid ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Inhibitory Effects ◽  
Cardiac Catheters ◽  
Response To Stress ◽  
Lh Secretion

Abstract Stress exerts profound inhibitory effects on reproductive function by suppressing the pulsatile release of GnRH and therefore LH. Although the mechanisms by which stressors disrupt the hypothalamic GnRH pulse generator remain to be fully elucidated, numerous studies have implicated the amygdala, especially its medial (MeA) and central nuclei (CeA), as key modulators of the neuroendocrine response to stress. In the present study, we investigated the roles of the MeA and CeA in stress-induced suppression of LH pulses. Ovariectomized rats received bilateral ibotenic acid or sham lesions targeting the MeA or CeA; blood samples (25 μl) were taken via chronically implanted cardiac catheters every 5 min for 6 h for the measurement of LH pulses. After 2 h of baseline sampling, the rats were exposed to either: restraint (1 h), insulin-induced hypoglycemia (IIH) (0.3 U/kg, iv), or lipopolysaccharide (LPS) (25 μg/kg, iv) stress. The restraint but not IIH or LPS stress–induced suppression of LH pulses was markedly attenuated by the MeA lesions. In contrast, CeA lesioning attenuated LPS, but not restraint or IIH stress–induced suppression of LH pulses. Moreover, after restraint stress, the number of Fos-positive neurons and the percentage of glutamic acid decarboxylase67 neurons expressing Fos was significantly greater in the GnRH-rich medial preoptic area (mPOA) of rats with intact, rather than lesioned, MeA. These data indicate that the MeA and CeA play key roles in psychogenic and immunological stress-induced suppression of the GnRH pulse generator, respectively, and the MeA-mediated effect may involve γ-aminobutyric acid ergic signaling within the mPOA.

scholarly journals Positive, But Not Negative Feedback Actions of Estradiol in Adult Female Mice Require Estrogen Receptor α in Kisspeptin Neurons

Endocrinology ◽  
2015 ◽  
Vol 156 (3) ◽  
pp. 1111-1120 ◽  
Author(s):  
Sharon L. Dubois ◽  
Maricedes Acosta-Martínez ◽  
Mary R. DeJoseph ◽  
Andrew Wolfe ◽  
Sally Radovick ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Adult Female ◽  
Negative Feedback ◽  
Positive Feedback ◽  
Estrogen Receptor Α ◽  
Female Mice ◽  
Lh Secretion ◽  
Express Estrogen Receptor ◽  
Specific Deletion

Abstract Hypothalamic kisspeptin (Kiss1) neurons express estrogen receptor α (ERα) and exert control over GnRH/LH secretion in female rodents. It has been proposed that estradiol (E2) activation of ERα in kisspeptin neurons in the arcuate nucleus (ARC) suppresses GnRH/LH secretion (negative feedback), whereas E2 activation of ERα in kisspeptin neurons in the anteroventral periventricular nucleus (AVPV) mediates the release of preovulatory GnRH/LH surges (positive feedback). To test these hypotheses, we generated mice bearing kisspeptin cell–specific deletion of ERα (KERαKO) and treated them with E2 regimens that evoke either negative or positive feedback actions on GnRH/LH secretion. Using negative feedback regimens, as expected, E2 effectively suppressed LH levels in ovariectomized (OVX) wild-type (WT) mice to the levels seen in ovary-intact mice. Surprisingly, however, despite the fact that E2 regulation of Kiss1 mRNA expression was abrogated in both the ARC and AVPV of KERαKO mice, E2 also effectively decreased LH levels in OVX KERαKO mice to the levels seen in ovary-intact mice. Conversely, using a positive feedback regimen, E2 stimulated LH surges in WT mice, but had no effect in KERαKO mice. These experiments clearly demonstrate that ERα in kisspeptin neurons is required for the positive, but not negative feedback actions of E2 on GnRH/LH secretion in adult female mice. It remains to be determined whether the failure of KERαKO mice to exhibit GnRH/LH surges reflects the role of ERα in the development of kisspeptin neurons, in the active signaling processes leading to the release of GnRH/LH surges, or both.

Effect of acute immunoneutralization of endogenous leptin on prolactin and LH secretion during the afternoon of pro-oestrus or in steroid-treated ovariectomized female rats

Reproduction ◽  
2000 ◽  
pp. 39-45 ◽  
Author(s):  
LC Gonzalez ◽  
L Pinilla ◽  
M Tena-Sempere ◽  
C Dieguez ◽  
FF Casanueva ◽  
...  
Keyword(s):  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Blood Samples ◽  
Lh Release ◽  
Lh Secretion

Recent data indicate that leptin is involved in the control of reproductive function. Experiments were carried out to analyse the role of endogenous leptin in the regulation of LH and prolactin secretion during the afternoon of pro-oestrus and that induced by ovarian steroids in ovariectomized rats. In the first experiment, cyclic female rats were implanted with intra-auricular and intracerebroventricular (i.c.v.) cannulae and, at pro-oestrus, were injected (i.c.v.) with 10 microliters normal rabbit serum or leptin antiserum (at 13:00 and 14:00 h). Blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the second experiment, female rats in pro-oestrus were injected with normal rabbit serum or leptin antiserum at 16:00 and 18:00 h and blood samples were taken every 10 min between 18:00 and 20:00 h. In the third experiment, adult female rats that had been ovariectomized 2 weeks before were implanted with intra-auricular and i.c.v. cannulae and treated with oestradiol benzoate (30 micrograms s.c.) at 10:00 h and progesterone (2 mg s.c.) 48 h later. Normal rabbit serum (10 microliters) or leptin antiserum (10 microliters) were injected (i.c.v.) at 13:00 and 14:00 h, and blood samples were obtained at 10:00 h and at intervals of 1 h between 13:00 and 20:00 h. In the fourth experiment, hemipituitaries from ovariectomized steroid-treated female rats were incubated in the presence of leptin116-130 (an active fragment of the native molecule), GnRH or leptin + GnRH. Prolactin and LH secretion during the afternoon of pro-oestrus in females treated with leptin antiserum was similar to that observed in animals injected with normal rabbit serum. In ovariectomized female rats, the steroid-induced LH surge increased slightly after administration of leptin antiserum, whereas the prolactin surge remained unchanged. In vitro, leptin116-130 (10(-5) to 10(-8) mol l-1) inhibited LH secretion and modulated the effect of GnRH on LH release, depending on the concentration of GnRH: leptin116-130 (10(-6) mol l-1) reduced the effectiveness of 10(-7) mol GnRH l-1 and increased that of 10(-9) mol GnRH l-1. In conclusion, these experiments indicate that acute immunoneutralization of endogenous leptin does not interfere with spontaneous or steroid-induced LH and prolactin surges. In addition, the finding that leptin116-130 inhibited LH release and modulated the effectiveness of GnRH in vitro provides evidence of the direct modulatory role of leptin on LH secretion acting at the pituitary.

scholarly journals Evidence for Ligand-Independent Activation of Hippocampal Estrogen Receptor-α by IGF-1 in Hippocampus of Ovariectomized Rats

Endocrinology ◽  
2016 ◽  
Vol 157 (8) ◽  
pp. 3149-3156 ◽  
Author(s):  
Elin M. Grissom ◽  
Jill M. Daniel
Keyword(s):  
Estrogen Receptor ◽  
Steroid Receptor ◽  
Estrogen Receptor Α ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Independent Manner ◽  
Steroid Receptor Coactivator ◽  
Intracerebroventricular Infusion

In the absence of ovarian estrogens, increased levels of estrogen receptor (ER)α in the hippocampus are associated with improvements in cognition. In vitro evidence indicates that under conditions of low estrogen, growth factors, including Insulin-Like Growth Factor 1 (IGF-1), can activate ERα and regulate ERα-mediated transcription through mechanisms that likely involve modification of phosphorylation sites on the receptor. The goal of the current work was to investigate a role for IGF-1 in ligand-independent activation of ERα in the hippocampus of female rats. Ovariectomized rats received a single intracerebroventricular infusion of IGF-1 and hippocampi were collected 1 or 24 hours later. After 1 h, IGF-1 increased hippocampal levels of phosphorylated ERα at serine 118 (S118) as revealed by Western blotting. Coimmunoprecipitation revealed that at 1 hour after infusion, IGF-1 increased association between ERα and steroid receptor coactivator 1, a histone acetyltransferase that increases transcriptional activity of phosphorylated ERα. IGF-1 infusion increased levels of the ERα-regulated proteins ERα, choline acetyltransferase, and brain-derived neurotrophic factor in the hippocampus 24 hours after infusion. Results indicate that IGF-1 activates ERα in ligand-independent manner in the hippocampus via phosphorylation at S118 resulting in increased association of ERα with steroid receptor coactivator 1 and elevation of ER-regulated proteins. To our knowledge, these data are the first in vivo evidence of ligand-independent actions of ERα and provide a mechanism by which ERα can impact memory in the absence of ovarian estrogens.

The role of estrogen receptor-α in estrogen-mediated regulation of basal and exercise-induced Hsp70 and Hsp27 expression in rat soleus

2013 ◽  
Vol 91 (10) ◽  
pp. 823-829 ◽  
Author(s):  
Eric Bombardier ◽  
Chris Vigna ◽  
Darin Bloemberg ◽  
Joe Quadrilatero ◽  
Peter M. Tiidus ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Alpha ◽  
Estrogen Receptor Α ◽  
Ovariectomized Rats ◽  
Type I ◽  
Type Ii ◽  
Mediated Effects ◽  
Exercise Induced ◽  
Shock Proteins

We examined the influence of estrogen receptor-alpha (ERα) activation on estrogen-mediated regulation of heat shock proteins 70 (Hsp70) and 27 (Hsp27) in soleus. Ovariectomized rats received estrogen (EST), an ERα agonist (propyl pyrazole triol, PPT), both (EST+PPT), or a sham, and they served as either unexercised controls or were subjected to exercise by having to run downhill (17 m/min, −13.5° grade) for 90 min. At 72 h postexercise, soleus muscles were removed and either immunohistochemically stained for Hsp70 and myosin heavy chain or homogenized for Western blotting for Hsp70 and Hsp27. Elevated (p < 0.05) basal Hsp70 in both type I and II fibres in the unexercised EST, PPT, and EST+PPT groups relative to unexercised sham animals was noted. Compared with Hsp70 levels in the unexercised animals, that in exercised animals was elevated (p < 0.05) in both sham and PPT groups but not in EST and EST+PPT groups. Western blot determined that Hsp27 levels were not significantly different between groups. Hence, the ability of estrogen to augment resting type I and type II muscle fibre Hsp70 content is primarily mediated via muscle ERα. However, the blunted Hsp70 response following damaging exercise in estrogen-supplemented animals does not appear to be fully accounted for by ERα-mediated effects.

scholarly journals Estrogen receptor-α prevents right ventricular diastolic dysfunction and fibrosis in female rats

2020 ◽  
Vol 319 (6) ◽  
pp. H1459-H1473
Author(s):  
Tik-Chee Cheng ◽  
Jennifer L. Philip ◽  
Diana M. Tabima ◽  
Santosh Kumari ◽  
Bakhtiyor Yakubov ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Right Ventricular ◽  
Diastolic Dysfunction ◽  
Pressure Overload ◽  
Estrogen Receptor Α ◽  
Female Rats ◽  
Loss Of Function ◽  
Ventricular Diastolic Dysfunction ◽  
Metalloproteinase 9

Using a novel loss-of-function mutation in estrogen receptor-α (ERα), we demonstrate that female, but not male, ERα mutant rats display right ventricular (RV)-vascular uncoupling, diastolic dysfunction, and fibrosis following pressure overload, indicating a sex-dependent role of ERα in protecting against adverse RV remodeling. TIMP metallopeptidase inhibitor 1 (Timp1), matrix metalloproteinase 9 (Mmp9), kallikrein-related peptidase 10 ( Klk10), and Jun Proto-Oncogene ( Jun) were identified as potential mediators in ERα-regulated pathways in RV pressure overload.

scholarly journals Involvement of Brainstem Catecholaminergic Inputs to the Hypothalamic Paraventricular Nucleus in Estrogen Receptor α Expression in this Nucleus during Different Stress Conditions in Female Rats

Endocrinology ◽  
2004 ◽  
Vol 145 (11) ◽  
pp. 4917-4926 ◽  
Author(s):  
Maria Amelita C. Estacio ◽  
Hiroko Tsukamura ◽  
Beverly A. S. Reyes ◽  
Yoshihisa Uenoyama ◽  
Helen I’Anson ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Paraventricular Nucleus ◽  
Estrogen Receptor Α ◽  
Stress Conditions ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Cell Group ◽  
Slight Reduction ◽  
Significant Difference ◽  
Cell Groups

Abstract In the present study, we determined the involvement of brainstem catecholaminergic inputs to the paraventricular nucleus (PVN) on estrogen receptor α (ERα) expression in this nucleus during conditions of 48-h fasting, 2-deoxy-d-glucose (2DG)-induced acute glucoprivation and 1-h immobilization, in ovariectomized rats. Our approach was to examine the effect of lesioning catecholaminergic inputs to the PVN using DSAP [saporin-conjugated anti-DBH (dopamine-β-hydroxylase)]. Bilateral injection of DSAP into the PVN, 2 wk before stress, prevented fasting-, glucoprivation-, and immobilization-induced increase in ERα-immunopositive cells in the PVN. The DBH-immunoreactive (ir) terminals in the PVN were severely depleted by DSAP injection in all experimental groups. Among the brainstem noradreneregic cell groups examined, DBH-ir cell bodies were significantly reduced in the A2 region of all experimental groups treated with DSAP compared with the saporin- and vehicle-injected controls. PVN DSAP injection caused a small, but not significant, decrease in A1 DBH-ir cell bodies in fasted and immobilized rats, and a significant, but slight, reduction in A1 DBH-ir cell bodies of iv 2DG- injected rats compared with PVN vehicle-injected or PVN saporin-injected controls. The A6 DBH-ir cell bodies in all experimental groups treated with DSAP, saporin, or vehicle did not show any significant difference. These results suggest that the brainstem catecholaminergic inputs to the PVN, especially from the A2 cell group, may play a major role in mediating the induction of ERα expression in the PVN by metabolic stressors such as fasting, acute glucoprivation, and less specific stressors, such as immobilization, in female rats.

Role of serotoninergic neurones in the control of gonadotrophin and prolactin secretion in the rat

1982 ◽  
Vol 94 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Csilla Ruzsas ◽  
Patrizia Limonta ◽  
L. Martini
Keyword(s):  
Combined Treatment ◽  
Prolactin Secretion ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Serum Prolactin ◽  
Intact Male ◽  
Prolactin Release ◽  
Lh Secretion ◽  
The Brain

The role of brain serotonin (5-hydroxytryptamine, 5-HT) in the control of LH, FSH and prolactin secretion was studied in two groups of experimental animals: intact adult male rats and ovariectomized adult female rats. 5-Hydroxytryptophan (5-HTP), a precursor of serotonin synthesis, and fluoxetine, a specific inhibitor of 5-HT uptake, were given either alone or together. 5-Hydroxytryptophan (50 mg/kg) was administered intraperitoneally and fluoxetine (20 μg/rat) was given into one of the lateral ventricles of the brain. Neither 5-HTP nor fluoxetine given alone affected LH secretion but combined treatment with the two drugs elicited a significant increase in serum LH levels in both intact male and ovariectomized female rats. Fluoxetine and 5-HTP, alone or together, did not modify FSH secretion in either kind of animal. In intact males and in ovariectomized females, 5-HTP induced a significant increase in prolactin release; fluoxetine alone was ineffective. In male animals treated with fluoxetine plus 5-HTP, serum prolactin levels increased but such an increase was lower than that found in the animals treated only with 5-HTP. In ovariectomized rats, the combined treatment induced an increase in serum prolactin levels similar to that found in animals treated with 5-HTP alone. These data suggested that brain serotonin exerts a stimulating effect on LH secretion in both intact male and ovariectomized rats, but that it does not play any role in the control of FSH release in either kind of animal and that central serotoninergic pathways participate in the stimulating control of prolactin release from the anterior pituitary gland. However, some of the data also suggested the possibility of the existence in the brain of serotoninergic systems inhibiting prolactin secretion.

Membrane estrogen receptor α is essential for estrogen signaling in the male skeleton

2018 ◽  
Vol 239 (3) ◽  
pp. 303-312 ◽  
Author(s):  
H H Farman ◽  
K L Gustafsson ◽  
P Henning ◽  
L Grahnemo ◽  
V Lionikaite ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Estrogen Receptor Α ◽  
Estrogen Signaling ◽  
Areal Bone Mineral Density ◽  
Male Mice ◽  
Mineral Density ◽  
Intact Male ◽  
Trabecular Thickness ◽  
Total Body

The importance of estrogen receptor α (ERα) for the regulation of bone mass in males is well established. ERα mediates estrogenic effects both via nuclear and membrane-initiated ERα (mERα) signaling. The role of mERα signaling for the effects of estrogen on bone in male mice is unknown. To investigate the role of mERα signaling, we have used mice (Nuclear-Only-ER; NOER) with a point mutation (C451A), which results in inhibited trafficking of ERα to the plasma membrane. Gonadal-intact male NOER mice had a significantly decreased total body areal bone mineral density (aBMD) compared to WT littermates at 3, 6 and 9 months of age as measured by dual-energy X-ray absorptiometry (DEXA). High-resolution microcomputed tomography (µCT) analysis of tibia in 3-month-old males demonstrated a decrease in cortical and trabecular thickness in NOER mice compared to WT littermates. As expected, estradiol (E2) treatment of orchidectomized (ORX) WT mice increased total body aBMD, trabecular BV/TV and cortical thickness in tibia compared to placebo treatment. E2 treatment increased these skeletal parameters also in ORX NOER mice. However, the estrogenic responses were significantly decreased in ORX NOER mice compared with ORX WT mice. In conclusion, mERα is essential for normal estrogen signaling in both trabecular and cortical bone in male mice. Increased knowledge of estrogen signaling mechanisms in the regulation of the male skeleton may aid in the development of new treatment options for male osteoporosis.

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