scholarly journals Estrogen and Estrogen Receptor-β (ERβ)-Selective Ligands Induce Galanin Expression within Gonadotropin Hormone-Releasing Hormone-Immunoreactive Neurons in the Female Rat Brain

Endocrinology ◽  
2005 ◽  
Vol 146 (6) ◽  
pp. 2760-2765 ◽  
Author(s):  
Istvan Merchenthaler ◽  
Gloria E. Hoffman ◽  
Malcolm V. Lane
Keyword(s):  
Ovariectomized Rats ◽  
Female Rat ◽  
Dependent Manner ◽  
Neuronal System ◽  
Selective Ligands ◽  
Gnrh Neurons ◽  
17Β Estradiol ◽  
Selective Agonists ◽  
The Many

Abstract Among the many factors that integrate the activity of the GnRH neuronal system, estrogens play the most important role. In females, estrogen, in addition to the negative feedback, also exhibits a positive feedback influence upon the activity and output of GnRH neurons to generate the preovulatory LH surge and ovulation. Until recently, the belief has been that the GnRH neurons do not contain estrogen receptors (ERs) and that the action of estrogen upon GnRH neurons is indirect involving several, estrogen-sensitive neurotransmitter and neuromodulator systems that trans-synaptically regulate the activity of the GnRH neurons. Based on our recent findings that GnRH neurons of the female rat coexpress galanin, that galanin is a potent GnRH-releasing peptide, and that ERβ is present in GnRH neurons, we have evaluated the effect of 17β-estradiol and two ERβ-selective agonists (WAY-200070, WAY-166818) on the expression of galanin within GnRH neurons. By combining immunocytochemistry for GnRH and in situ hybridization histochemistry for galanin, we demonstrate that 17β-estradiol (20 μg/kg, sc) stimulates galanin expression within GnRH-immunoreactive neurons in a time-dependent manner. A significant increase was observed 2 h after its administration to ovariectomized rats. However, a more robust expression required 3-d treatment regimen. Treatment with the β-selective ligands resulted in similar observations, although no statistical analysis is available for the 2 hr survival. These observations strongly suggest that estrogen and the ERβ-selective ligands stimulate galanin expression within GnRH neurons via ERβ, although an indirect mechanism via interneurons still cannot be ruled out.

scholarly journals The influence of 17β-estradiol on annexin 1 expression in the anterior pituitary of the female rat and in a folliculo-stellate cell line

2007 ◽  
Vol 192 (2) ◽  
pp. 429-442 ◽  
Author(s):  
Evelyn Davies ◽  
Selma Omer ◽  
John F Morris ◽  
Helen C Christian
Keyword(s):  
Cell Line ◽  
Estrous Cycle ◽  
Anterior Pituitary ◽  
Stellate Cell ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Annexin 1 ◽  
17Β Estradiol ◽  
Estrous Cycle Stage

Annexin 1 (ANXA1) is a Ca2+- and phospholipid-binding protein that plays an important role as a mediator of glucocorticoid action in the host-defence and neuroendocrine systems. Sex differences in hypothalamo–pituitary–adrenal (HPA) axis activity are well documented and a number of studies have demonstrated that gonadal steroids act as regulators of HPA activity. The aim of this study was to investigate the effect of ovariectomyand 17β-estradiol replacement, and estrous cycle stage, on anterior pituitary ANXA1 content. The amount of anterior pituitary ANXA1 determined by western blotting varied with estrous cycle stage with a peak at estrus declining to a trough at proestrus. Ovariectomy resulted in a significant (P<0.05) decrease in anterior pituitary ANXA1 content. Administration of 17β-estradiol (1 μg/100 g) significantly (P<0.01) increased anterior pituitary ANXA1 expression in the ovariectomized animals. In contrast, there was no change in pituitary ANXA1 content in response to 17β-estradiol in adrenalectomized and adrenalectomized/ovariectomized rats. Treatment of TtT/GF cells, a folliculo-stellate cell line, with 17β-estradiol (1.8–180 nM) increased ANXA1 mRNA expression and increased the amount of ANXA1 protein externalized in response to a dexamethasone stimulus. These results indicate that 17β-estradiol stimulates ANXA1 expression in the anterior pituitary and in vivo an adrenal factor contributes to the mechanism of action.

scholarly journals Hypothalamic Prolactin Receptor Messenger Ribonucleic Acid Levels, Prolactin Signaling, and Hyperprolactinemic Inhibition of Pulsatile Luteinizing Hormone Secretion Are Dependent on Estradiol

Endocrinology ◽  
2007 ◽  
Vol 149 (4) ◽  
pp. 1562-1570 ◽  
Author(s):  
Greg M. Anderson ◽  
David C. Kieser ◽  
Frederick J. Steyn ◽  
David R. Grattan
Keyword(s):  
Hormone Secretion ◽  
Pulse Frequency ◽  
Ovariectomized Rats ◽  
Cytokine Signaling ◽  
Dopamine Antagonist ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Lh Surge ◽  
Prolactin Signaling ◽  
Gnrh Neurons

Hyperprolactinemia can reduce fertility and libido. Although central prolactin actions are thought to contribute to this, the mechanisms are poorly understood. We first tested whether chronic hyperprolactinemia inhibited two neuroendocrine parameters necessary for female fertility: pulsatile LH secretion and the estrogen-induced LH surge. Chronic hyperprolactinemia induced by the dopamine antagonist sulpiride caused a 40% reduction LH pulse frequency in ovariectomized rats, but only in the presence of chronic low levels of estradiol. Sulpiride did not affect the magnitude of a steroid-induced LH surge or the percentage of GnRH neurons activated during the surge. Estradiol is known to influence expression of the long form of prolactin receptors (PRL-R) and components of prolactin’s signaling pathway. To test the hypothesis that estrogen increases PRL-R expression and sensitivity to prolactin, we next demonstrated that estradiol greatly augments prolactin-induced STAT5 activation. Lastly, we measured PRL-R and suppressor of cytokine signaling (SOCS-1 and -3 and CIS, which reflect the level of prolactin signaling) mRNAs in response to sulpiride and estradiol. Sulpiride induced only SOCS-1 in the medial preoptic area, where GnRH neurons are regulated, but in the arcuate nucleus and choroid plexus, PRL-R, SOCS-3, and CIS mRNA levels were also induced. Estradiol enhanced these effects on SOCS-3 and CIS. Interestingly, estradiol also induced PRL-R, SOCS-3, and CIS mRNA levels independently. These data show that GnRH pulse frequency is inhibited by chronic hyperprolactinemia in a steroid-dependent manner. They also provide evidence for estradiol-dependent and brain region-specific regulation of PRL-R expression and signaling responses by prolactin.

scholarly journals New Perspectives for Anatomical and Molecular Studies of Kisspeptin Neurons in the Aging Human Brain

2019 ◽  
Vol 109 (3) ◽  
pp. 230-241 ◽  
Author(s):  
Erik Hrabovszky ◽  
Szabolcs Takács ◽  
Balázs Göcz ◽  
Katalin Skrapits
Keyword(s):  
Arcuate Nucleus ◽  
Anatomical Site ◽  
Neuronal System ◽  
Hormone Signaling ◽  
Neurokinin B ◽  
Molecular Approaches ◽  
Endocrine Organs ◽  
Aging Men ◽  
Gnrh Neurons

The human infundibular nucleus (corresponding to the rodent arcuate nucleus) serves as an important integration center for neuronal signals and hormones released by peripheral endocrine organs. Kisspeptin (KP)-producing neurons of this anatomical site, many of which also synthesize neurokinin B (NKB), are critically involved in sex hormone signaling to gonadotropin-releasing hormone (GnRH) neurons. In recent years, the basic topography, morphology, neuropeptide content, and connectivity of human KP neurons have been investigated with in situ hybridization and immunohistochemistry on postmortem tissues. These studies revealed that human KP neurons differ neurochemically from their rodent counterparts and show robust aging-related plasticity. Earlier immunohistochemical experiments also provided evidence for temporal changes in the hypothalamus of aging men whose NKB and KP neurons undergo hypertrophy, increase in number, exhibit increased neuropeptide mRNA expression and immunoreactivity and give rise to higher numbers of immunoreactive fibers and afferent contacts onto GnRH neurons. Increasing percentages of KP-expressing NKB perikarya, NKB axons, and NKB inputs to GnRH neurons raise the intriguing possibility that a significant subset of NKB neurons begins to cosynthesize KP as aging advances. Although use of postmortem tissues is technically challenging, recently available single-cell anatomical and molecular approaches discussed in this review provide promising new tools to investigate the aging-related anatomical and functional plasticity of the human KP neuronal system.

Estradiol modulates vascular response to melatonin in rat caudal artery

1999 ◽  
Vol 276 (4) ◽  
pp. H1281-H1288 ◽  
Author(s):  
Suzanne Doolen ◽  
Diana N. Krause ◽  
Sue P. Duckles
Keyword(s):  
Estrous Cycle ◽  
Melatonin Receptors ◽  
Female Rats ◽  
Adrenergic Nerve ◽  
Receptor Subtypes ◽  
Female Rat ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Caudal Artery ◽  
17Β Estradiol

The purpose of this study was to determine whether estrogen modulates the function of vascular melatonin receptors. We used the rat caudal artery and found that the contractile effects of melatonin were influenced by the estrous cycle, ovariectomy, and estrogen replacement. In arterial ring segments isolated from female rats, melatonin potentiated, in a concentration-dependent manner, contractions produced either by adrenergic nerve stimulation or by phenylephrine. Constrictor responses to melatonin were smaller in arteries from female rats in proestrus compared with other stages of the estrous cycle and after ovariectomy. Administration of 17β-estradiol to ovariectomized female rats also resulted in decreased constriction of isolated arteries to melatonin; however, in vitro addition of 17β-estradiol (10−7 M) had no effect. In the caudal artery, melatonin appears to act on two receptor subtypes that mediate contraction and relaxation, respectively. The selective melatonin MT2-receptor antagonist 4-phenyl-2-propionamidotetraline (4P-PDOT) enhanced constrictor responses to melatonin in arterial segments from intact female rats, consistent with the inhibition of MT2 receptor-mediated relaxation. In contrast, 4P-PDOT had no significant effect in arteries from ovariectomized female rats. However, when estradiol was replaced in vivo, the effect of 4P-PDOT on melatonin responses was restored. Thus circulating estradiol appears to enhance MT2 melatonin-receptor function in the thermoregulatory caudal artery of the female rat resulting in increased vasodilatation in response to melatonin.

Soleus muscle force following downhill running in ovariectomized rats treated with estrogen

2006 ◽  
Vol 31 (4) ◽  
pp. 449-459 ◽  
Author(s):  
Sofia Sotiriadou ◽  
Antonios Kyparos ◽  
Maria Albani ◽  
Georgios Arsos ◽  
Mark S.F. Clarke ◽  
...  
Keyword(s):  
Soleus Muscle ◽  
Muscle Injury ◽  
Ovariectomized Rats ◽  
Tetanic Force ◽  
Downhill Running ◽  
Ovx Rats ◽  
17Β Estradiol ◽  
Maximal Tetanic Force ◽  
40 Hz

The ovariectomized (OVX) rat model was used to investigate the effects of estrogen treatment on soleus muscle functionality in situ following muscle injury induced by downhill running. Fifty immature, 24- to 26-d-old, OVX rats were randomly assigned to 5 separate experimental groups: sedentary controls (OVX-Sed), placebo-treated and studied immediately after exercise (OVX-Pb0), placebo-treated and studied 72 h after exercise (OVX-Pb72), estradiol-treated and studied immediately after exercise (OVX-Ed0), and estradiol-treated and studied 72 h after exercise (OVX-Ed72). At the age of 9 weeks, under ketamine and xylazine anesthesia i.p., the rats were subcutaneously implanted with either placebo or 17β-estradiol-impregnated pellets (0.05 mg/pellet, 3 week release). Treatment with 17β-estradiol increased the estradiol plasma levels in OVX animals to those normally seen during the proestrous cycle of normal animals. Three weeks after the implantation the rats were subjected to a 90 min intermittent downhill running protocol. Our results indicate that the exercise protocol used in the study induced injury in the soleus muscle, as it was detected by the significant reduction in unfused (stimulation at 10, 20, and 40 Hz) and maximal (Po) tetanic force, as well as the decreased ability of the soleus muscle to maintain tension (stimulation at 40 Hz for 3 min) in OVX-Pb0 and OVX-Pb72 placebo-treated animals subjected to downhill running (injured muscles) as compared with OVX-Sed control rats (uninjured muscle). Estradiol replacement in OVX rats partially protected the soleus muscle from the injury normally induced by downhill running. As compared with the OVX-Pb0 and OVX-Pb72 placebo-treated groups, the soleus muscles of OVX-Ed0 and OVX-Ed72 estradiol-treated rats were capable of producing significantly greater unfused tetanic force and had an increased ability to maintain tension after fatigue. However, estrogen at the dose administered did not prevent the decrease in maximal tetanic force. We postulate that the protective effect of estrogens on muscle strength may be related to the ability of estrogen hormones to attenuate the E–C coupling failure and (or) the disorganization of the contractile apparatus associated with eccentric exercise through a mechanism or mechanisms yet to be fully understood.

17β-Estradiol deficiency reduces potassium excretion in an angiotensin type 1 receptor-dependent manner

2007 ◽  
Vol 293 (1) ◽  
pp. H17-H22 ◽  
Author(s):  
Hong Ji ◽  
Wei Zheng ◽  
Celine Falconetti ◽  
Darren M. Roesch ◽  
Susan E. Mulroney ◽  
...  
Keyword(s):  
Renal Function ◽  
Enzyme Inhibitor ◽  
Binding Capacity ◽  
Fractional Excretion ◽  
Ovariectomized Rats ◽  
Dependent Manner ◽  
Potassium Excretion ◽  
Sprague Dawley ◽  
17Β Estradiol

This study examined the effects of ovariectomy (OVX) and 17β-estradiol (E2) replacement (OVX + E2) on renal function in Sprague-Dawley rats. OVX caused a 40% decrease in the fractional excretion of potassium (FEK+) that was prevented by E2 replacement [Sham, 24.2 ± 2.9%; OVX, 14.5 ± 2.1% ( P < 0.05 vs. OVX + E2); and OVX + E2, 26.2 ± 2.7%; n = 7–11] and that corresponded to significant increases in plasma potassium [(in mmol/l): Sham, 3.15 ± 0.087; OVX, 3.42 ± 0.048 ( P < 0.05 vs. OVX + E2); and OVX + E2, 3.19 ± 0.11; n = 7–11]. No effects of OVX were detected on plasma levels of sodium and aldosterone. Angiotensin II type 1 receptor (AT1R) densities in ovariectomized rats were 1.4-fold and 1.3-fold higher in glomerular [maximum binding capacity (Bmax; in fmol/mg protein): Sham, 482 ± 21; OVX, 666 ± 20 ( P < 0.05 vs. OVX + E2); and OVX + E2, 504 ± 26; n = 7–11] and proximal tubular [Bmax (in fmol/mg protein): Sham, 721 ± 16; OVX, 741 ± 24 ( P < 0.05 vs. OVX + E2); and OVX + E2, 569 ± 23; n = 7–11] membranes compared with E2 replete animals, respectively. Both the angiotensin-converting enzyme inhibitor captopril and the AT1R antagonist losartan prevented the OVX-induced decrease in the FEK+ and the increase in renal AT1R densities, suggesting that E2 deficiency reduces potassium excretion in an ANG II/AT1R-dependent manner. These findings may have implications for renal function in postmenopausal women as well as contribute to the reasons underlying the age-induced increase in susceptibility to hypertension-associated disease in women.

scholarly journals The Role of the Locus Coeruleus in Corticotropin-Releasing Hormone and Stress-Induced Suppression of Pulsatile Luteinizing Hormone Secretion in the Female Rat

Endocrinology ◽  
2005 ◽  
Vol 146 (1) ◽  
pp. 323-331 ◽  
Author(s):  
J. C. Mitchell ◽  
X. F. Li ◽  
L. Breen ◽  
J.-C. Thalabard ◽  
K. T. O’Byrne
Keyword(s):  
Glutamic Acid ◽  
Locus Coeruleus ◽  
Stress Responses ◽  
Pulse Generator ◽  
Critical Role ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Central Administration ◽  
17Β Estradiol ◽  
Lh Secretion

Despite a wealth of evidence for CRH mediating stress-induced suppression of the hypothalamic GnRH pulse generator, and hence reproductive dysfunction, the site and mechanism of action remains elusive. The locus coeruleus (LC), a prominent noradrenergic brain stem nucleus, is innervated by CRH neurons, mediates several behavioral stress responses, and is implicated in the control of pulsatile LH secretion. The aim of this study was to test the hypothesis that LC CRH has a critical role in mediating stress-induced suppression of pulsatile LH secretion in the rat. Ovariectomized rats with 17β-estradiol or oil-filled sc capsules were implanted with bilateral LC and iv cannulae. Central administration of CRH (10 ng to 1 μg) resulted in a dose-dependent suppression of LH pulses, which was reversed by a CRH receptor antagonist (α-helical CRF9–41, 1 μg). The induction of c-fos expression in glutamic acid decarboxylase67 immunostained neurons in the preoptic area suggests activation of the secretion of γ-aminobutyric acid in response to intracoerulear administration of CRH; 17β-estradiol further increased the percentage of glutamic acid decarboxylase67-positive neurons that expressed fos and augmented suppression of LH pulses. Furthermore, intracoerulear administration of α-helical CRF9–41 completely blocked restraint stress-induced suppression of LH pulses, without affecting the inhibitory response to hypoglycemia. These results suggest that CRH innervation of the LC may play a pivotal, but differential, role in the normal physiological response of stress-induced suppression of the GnRH pulse generator and hence the reproductive system.

DEVELOPMENT OF OVARIAN AUTOGRAFTS ON THE GREATER OMENTUM OF OVARIECTOMIZED AND HEMI-OVARIECTOMIZED RATS UNITED BY COELIO-ANASTOMOSIS

1971 ◽  
Vol 68 (1) ◽  
pp. 50-58
Author(s):  
Artur Ber
Keyword(s):  
Mortality Rate ◽  
Good Health ◽  
Ovariectomized Rats ◽  
Greater Omentum ◽  
Female Rat ◽  
Small Decrease ◽  
The Mean

ABSTRACT Ovariectomized and hemi-ovariectomized 3 week old non-littermate rats bearing ovarian implants on the greater omentum were parabiosed by coelio-anastomosis. Controls consisted of 67 spayed and 58 hemi-spayed single animals with similar ovarian implants. To each pair of parabionts an older female rat served as »nurse« keeping them in relatively good health; the mortality rate, nevertheless reached about 20 %. After one month 15 parabiotic pairs and all the control animals were killed. In the hemi-spayed parabionts the mean weights of the uteri and ovaries in situ were significantly higher than in single control animals while the rise in the mean pituitary weight was not significant. The mean weight of the implants was the same as in the control rats. In the spayed parabionts the mean weights of the uteri and pituitaries were significantly higher than in single control rats. The small decrease in the mean weight of the implants was not statistically significant. The results obtained show that oestrogens passed from the hemi-spayed to the spayed animals probably causing inter alia, a decrease in gonadotrophin production and release. The amount of gonadotrophins passing from the spayed to the hemi-spayed partners was, however, sufficient to influence the development of the ovaries and uteri. In contrast, the development of the ovarian implants was not stimulated. This discrepancy confirms the assumption that the ovary in situ produces a substance which inhibits gonadotrophic activity at the level of the implant.

scholarly journals 17β-Estradiol Exacerbated Experimental Occlusal Interference-Induced Chronic Masseter Hyperalgesia by Increasing the Neuronal Excitability and TRPV1 Function of Trigeminal Ganglion in Ovariectomized Rats

2021 ◽  
Vol 22 (13) ◽  
pp. 6945
Author(s):  
Yun Liu ◽  
Xiao-Xiang Xu ◽  
Ye Cao ◽  
Si-Yi Mo ◽  
Shan-Shan Bai ◽  
...  
Keyword(s):  
Trigeminal Ganglion ◽  
Transient Receptor Potential ◽  
Neuronal Excitability ◽  
Mechanical Hyperalgesia ◽  
Ovariectomized Rats ◽  
Facilitatory Effect ◽  
Transient Receptor Potential Vanilloid ◽  
Dependent Manner ◽  
Ovx Rats ◽  
17Β Estradiol

Pain symptoms in temporomandibular disorders (TMD) predominantly affect reproductive women, suggesting that estrogen regulates pain perception. However, how estrogen contributes to chronic TMD pain remains largely unclear. In the present study, we performed behavioral tests, electrophysiology, Western blot and immunofluorescence to investigate the role and underlying mechanisms of estrogen in dental experimental occlusal interference (EOI)-induced chronic masseter mechanical hyperalgesia in rats. We found that long-term 17β-estradiol (E2) replacement exacerbated EOI-induced masseter hyperalgesia in a dose-dependent manner in ovariectomized (OVX) rats. Whole-cell patch-clamp recordings demonstrated that E2 (100 nM) treatment enhanced the excitability of isolated trigeminal ganglion (TG) neurons in OVX and OVX EOI rats, and EOI increased the functional expression of transient receptor potential vanilloid-1 (TRPV1). In addition, E2 replacement upregulated the protein expression of TRPV1 in EOI-treated OVX rats. Importantly, intraganglionic administration of the TRPV1 antagonist AMG-9810 strongly attenuated the facilitatory effect of E2 on EOI-induced masseter mechanical sensitivity. These results demonstrate that E2 exacerbated EOI-induced chronic masseter mechanical hyperalgesia by increasing TG neuronal excitability and TRPV1 function. Our study helps to elucidate the E2 actions in chronic myogenic TMD pain and may provide new therapeutic targets for relieving estrogen-sensitive pain.

POSSIBLE ROLE OF 5α-ANDROSTANE-3α,17β-DIOL IN THE CONTROL OF FOLLICLE-STIMULATING HORMONE SECRETION IN THE IMMATURE FEMALE RAT

1982 ◽  
Vol 92 (1) ◽  
pp. 37-42 ◽  
Author(s):  
H. M. A. MEIJS-ROELOFS ◽  
P. KRAMER ◽  
L. GRIBLING-HEGGE
Keyword(s):  
Inhibitory Action ◽  
Combined Treatment ◽  
Hormone Secretion ◽  
Inhibitory Effect ◽  
Ovariectomized Rats ◽  
Female Rat ◽  
Immature Rat ◽  
Rat Strain ◽  
Intact Rats

A possible role of 5α-androstane-3α,17β-diol (3α-androstanediol) in the control of FSH secretion was studied at various ages in ovariectomized rats. In the rat strain used, vaginal opening, coincident with first ovulation, generally occurs between 37 and 42 days of age. If 3α-androstanediol alone was given as an ovarian substitute, an inhibitory effect on FSH release was evident with all three doses tested (50, 100, 300 μg/100 g body wt) between 13 and 30 days of age; at 33–35 days of age only the 300 μg dose caused some inhibition of FSH release. Results were more complex if 3α-androstanediol was given in combined treatment with oestradiol and progesterone. Given with progesterone, 3α-androstanediol showed a synergistic inhibitory action on FSH release between 20 and 30 days of age. However, when 3α-androstanediol was combined with oestradiol a clear decrease in effect, as compared to the effect of oestradiol alone, was found between 20 and 30 days of age. Also the effect of combined oestradiol and progesterone treatment was greater than the effect of combined treatment with oestradiol, progesterone and 3α-androstanediol. At all ages after day 20 none of the steroid combinations tested was capable of maintaining FSH levels in ovariectomized rats similar to those in intact rats. It is concluded that 3α-androstanediol might play a role in the control of FSH secretion in the immature rat, but after day 20 the potentially inhibitory action of 3α-androstanediol on FSH secretion is limited in the presence of oestradiol.

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