Artykuły w czasopismach: „Gonadotropin releasing hormone – Receptors”

1

Braden, Tim D., i P. Michael Conn. "The 1990 James A. F. Stevenson Memorial Lecture. Gonadotropin-releasing hormone and its actions". Canadian Journal of Physiology and Pharmacology 69, nr 4 (1.04.1991): 445–58. http://dx.doi.org/10.1139/y91-067.

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Gonadotropin-releasing hormone (GnRH) stimulates the release and biosynthesis of gonadotropins, luteinizing hormone, and follicle-stimulating hormone from the pituitary gland. Additionally, GnRH regulates the number of its own receptors on pituitary gonadotropes causing both up- and down-regulation of receptors as well as biosynthesis of GnRH receptors. After exposure to GnRH, gonadotropes become desensitized to further stimulation by GnRH. The mechanisms through which these actions of GnRH are mediated appear to differ. Effects dependent upon extracellular calcium include gonadotropin biosynthesis and release as well as up-regulation of GnRH receptors. Additional actions of GnRH, such as down-regulation of receptors, biosynthesis of receptors, and desensitization, appear to be independent of extracellular calcium. Subsequent studies have ascribed roles for calmodulin and protein kinase C in mediating specific effects of GnRH.Key words: pituitary, gonadotropin-releasing hormone, receptor, protein kinase C, calmodulin.

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Millar, Robert P., Zhi-Liang Lu, Adam J. Pawson, Colleen A. Flanagan, Kevin Morgan i Stuart R. Maudsley. "Gonadotropin-Releasing Hormone Receptors". Endocrine Reviews 25, nr 2 (1.04.2004): 235–75. http://dx.doi.org/10.1210/er.2003-0002.

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Carriere, Paul D., Riaz Farookhi i James R. Brawer. "The role of aberrant hypothalamic opiatergc function in generating polycystic ovaries in the rat". Canadian Journal of Physiology and Pharmacology 67, nr 8 (1.08.1989): 896–901. http://dx.doi.org/10.1139/y89-140.

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Treatment of adult female rats with estradiol valerate produces an intractable hypothalamic impairment that ultimately results in anovulatory acyclicity and polycystic ovaries. Evidence from our laboratory suggests that the hypothalamic impairment compromises regulation of the endogenous opioid system engendering a persistent opiatergic suppression of gonadotropin-releasing hormone secretion, which is subsequently reflected in a chronically low pituitary content of gonadotropin-releasing hormone receptors. If such is the case, inhibition of opiatergic transmission should improve the gonadotropin-releasing hormone pattern resulting in an improvement in the pituitary content of gonadotropin-releasing hormone receptors, and in an amelioration of the polycystic condition. We, therefore, treated rats with the polycystic ovarian condition, with daily injections of naltrexone. Within 1 week, there was a significant increase in the pituitary content of gonadotropin-releasing hormone receptors and a marked improvement in ovarian morphology, indicating that the hypothalamic opiatergic system is chronically active, and contributes significantly to the polycystic ovarian condition.Key words: hypothalamus, opiates, infertility, ovary, polycystic ovaries.

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Davidson, J. S., I. K. Wakefield i R. P. Millar. "Absence of rapid desensitization of the mouse gonadotropin-releasing hormone receptor". Biochemical Journal 300, nr 2 (1.06.1994): 299–302. http://dx.doi.org/10.1042/bj3000299.

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Desensitization of gonadotropin release by the pituitary gland in response to gonadotropin-releasing hormone (GnRH) agonists has clinical applications in the treatment of gonadal-hormone-dependent disorders. We therefore investigated possible desensitization of inositol phosphate (IP) responses of GNRH receptors. No short-term homologous desensitization of the IP response to GnRH was observed in either alpha T3 gonadotrope cells line or GH3 cells transfected with GnRH receptor cDNA. The absence of homologous desensitization is unusual among G-protein-coupled receptors, and may be due to the absence of a C-terminal cytoplasmic tail, a unique feature of the GnRH receptor. Several potential protein kinase C phosphorylation sites which might mediate heterologous desensitization are present on the GnRH receptor. In both alpha T3 cells and GnRH-receptor-transfected Cos-1 cells, activation of protein kinase C by pretreatment with phorbol ester caused a 35-53% decrease in the IP response to GnRH. However, phorbol ester also inhibited guanosine 5′-[gamma-thio]triphosphate-stimulated IP production in permeabilized Cos-1 cells, suggesting that this inhibition is mediated at a post-receptor site.

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KATT, J. A., J. A. DUNCAN, L. HERBON, A. BARKAN i J. C. MARSHALL. "THE FREQUENCY OF GONADOTROPIN-RELEASING HORMONE STIMULATION DETERMINES THE NUMBER OF PITUITARY GONADOTROPIN-RELEASING HORMONE RECEPTORS". Endocrinology 116, nr 5 (maj 1985): 2113–15. http://dx.doi.org/10.1210/endo-116-5-2113.

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Sedgley, Kathleen R., Ann R. Finch, Christopher J. Caunt i Craig A. McArdle. "Intracellular gonadotropin-releasing hormone receptors in breast cancer and gonadotrope lineage cells". Journal of Endocrinology 191, nr 3 (grudzień 2006): 625–36. http://dx.doi.org/10.1677/joe.1.07067.

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Gonadotropin-releasing hormone receptors (GnRHRs) are expressed in gonadotropes and several extra-pituitary sites. They are assumed to be cell surface proteins but the human (h) GnRHR lacks features favoring plasma membrane localization and receptor location varies with cell type. When expressed in mammary (MCF7) cells, cell surface hGnRHR binding was much lower than that of mouse and sheep GnRHRs (type I GnRHRs without C-terminal tails), Xenopus (X) and marmoset type II GnRHRs (type II GnRHRs with C-tails) or chimeric receptors (type I GnRHRs with added XGnRHR C-tails). hGnRHR binding was higher in αT4 (gonadotrope-derived) cells and was increased less by C-tail addition. Whole cell levels of tagged human, Xenopus and chimeric GnRHRs were comparable (Western blotting) and confocal microscopy revealed that the hGnRHR is primarily intracellular (distribution similar to the endoplasmic reticulum marker, calreticulin), whereas most XGnRHR is at the plasma membrane, and adding the C-tail increased cell surface hGnRHR levels. A membrane-permeant antagonist increased cell surface hGnRHR number (>4-fold, t½ = 4 h) and also increased hGnRHR signaling and hGnRHR-mediated inhibition of proliferation. A more rapid increase in hGnRHR binding occurred when the temperature was raised from 4 to 37 °C (>5-fold, t½ = 15 min) and this effect was prevented by mutation to prevent signaling. Thus, cell surface GnRHR expression depends on receptor and cell type and the hGnRHR is primarily an intracellular protein that traffics to the cell surface for signaling in MCF7 cells. Manipulations favoring such trafficking may facilitate selective targeting of extra-pituitary GnRHRs.

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Gründker, Carsten, i Günter Emons. "Role of Gonadotropin-Releasing Hormone (GnRH) in Ovarian Cancer". Cells 10, nr 2 (18.02.2021): 437. http://dx.doi.org/10.3390/cells10020437.

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The hypothalamus–pituitary–gonadal (HPG) axis is the endocrine regulation system that controls the woman’s cycle. The gonadotropin-releasing hormone (GnRH) plays the central role. In addition to the gonadotrophic cells of the pituitary, GnRH receptors are expressed in other reproductive organs, such as the ovary and in tumors originating from the ovary. In ovarian cancer, GnRH is involved in the regulation of proliferation and metastasis. The effects on ovarian tumors can be indirect or direct. GnRH acts indirectly via the HPG axis and directly via GnRH receptors on the surface of ovarian cancer cells. In this systematic review, we will give an overview of the role of GnRH in ovarian cancer development, progression and therapy.

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Brothers, Shaun P., Jo Ann Janovick i P. Michael Conn. "Calnexin regulated gonadotropin-releasing hormone receptor plasma membrane expression". Journal of Molecular Endocrinology 37, nr 3 (grudzień 2006): 479–88. http://dx.doi.org/10.1677/jme.1.02142.

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A significant proportion of human gonadotropin-releasing hormone receptors (GnRHRs) are normally retained in the endoplasmic reticulum (ER); however, nearly all rat GnRHRs are routed to the plasma membrane. When mutations are introduced into either receptor, considerably more of the proteins are recognized by the quality control system (QCS) as misfolded and retained compared with wild-type (WT) receptor, resulting in decreased signaling in the presence of agonist. Calnexin, a component of the QCS, decreased plasma membrane expression of the GnRHRs, an effect that was mediated by a physical interaction between the receptor and the calnexin. Only the human receptor showed reduced signaling because it had fewer spare receptors compared with the rat GnRHR, allowing calnexin to affect signaling. Calnexin did not affect receptor signaling when K191 was deleted from the human WT GnRHR. Removal of this amino acid decreases receptor misfolding and increases plasma membrane expression. K191 is not present in the rat WT GnRHR. A pharmacological chaperone that corrects GnRHR misfolding, increased expression of the human WT GnRHR in the presence of calnexin. Calnexin apparently retains misfolded GnRHRs but routes correctly folded receptors to the plasma membrane. Mutation of a calnexin protein kinase C consensus phosphorylation site promoted increased retention of the human GnRHR, suggesting that calnexin phosphorylation controls the retention mechanism. We conclude that a proportion of the human and the rat WT GnRHR appears to be retained in the ER by calnexin, an effect that decreases GnRHR signaling capacity.

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Xu, Peng, Yuhua Jia, Yongshuai Yang, Jincan Chen, Ping Hu, Zhuo Chen i Mingdong Huang. "Photodynamic Oncotherapy Mediated by Gonadotropin-Releasing Hormone Receptors". Journal of Medicinal Chemistry 60, nr 20 (10.10.2017): 8667–72. http://dx.doi.org/10.1021/acs.jmedchem.7b01216.

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Parhar, Ishwar S. "Gonadotropin-releasing hormone receptors: neuroendocrine regulators and neuromodulators". Fish Physiology and Biochemistry 28, nr 1-4 (2003): 13–18. http://dx.doi.org/10.1023/b:fish.0000030462.10997.24.

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Finch, Ann R., Christopher J. Caunt, Stephen P. Armstrong i Craig A. McArdle. "Agonist-induced internalization and downregulation of gonadotropin-releasing hormone receptors". American Journal of Physiology-Cell Physiology 297, nr 3 (wrzesień 2009): C591—C600. http://dx.doi.org/10.1152/ajpcell.00166.2009.

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Gonadotropin-releasing hormone (GnRH) acts via seven transmembrane receptors to stimulate gonadotropin secretion. Sustained stimulation desensitizes GnRH receptor (GnRHR)-mediated gonadotropin secretion, and this underlies agonist use in hormone-dependent cancers. Since type I mammalian GnRHR do not desensitize, agonist-induced internalization and downregulation may underlie desensitization of GnRH-stimulated gonadotropin secretion; however, research focus has recently shifted to anterograde trafficking, with the finding that human (h)GnRHR are mostly intracellular. Moreover, there is little direct evidence for agonist-induced trafficking of hGnRHR, and whether or not type I mammalian GnRHR show agonist-induced internalization is controversial. Here we use automated imaging to monitor expression and internalization of hemagglutinin (HA)-tagged hGnRHRs, mouse (m) GnRHR, Xenopus (X) GnRHRs, and chimeric receptors (hGnRHR with added XGnRHR COOH tails, h.XGnRHR) expressed by adenoviral transduction in HeLa cells. We find that agonists stimulate downregulation and/or internalization of mGnRHR and XGnRHR, that GnRH stimulates trafficking of hGnRHR and can stimulate internalization or downregulation of hGnRHR when steps are taken to increase cell surface expression (addition of the XGnRHR COOH tail or pretreatment with pharmacological chaperone). Agonist effects on internalization (of h.XGnRHR) and downregulation (of hGnRHR and h.XGnRHR) were not mimicked by a peptide antagonist and were prevented by a mutation that prevents GnRHR signaling, demonstrating dependence on receptor signaling as well as agonist occupancy. Thus agonist-induced internalization and downregulation of type I mammalian GnRHR occurs in HeLa cells, and we suggest that the high throughput imaging systems described here will facilitate study of the molecular mechanisms involved.

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Millar, RP, PJ Wormald i RC Milton. "Stimulation of gonadotropin release by a non-GnRH peptide sequence of the GnRH precursor". Science 232, nr 4746 (4.04.1986): 68–70. http://dx.doi.org/10.1126/science.3082009.

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The human gonadotropin-releasing hormone (GnRH) precursor comprises the GnRH sequence followed by an extension of 59 amino acids. Basic amino acid residues in the carboxyl terminal extension may represent sites of processing to biologically active peptides. A synthetic peptide comprising the first 13 amino acids (H X Asp-Ala-Glu-Asn-Leu-Ile-Asp-Ser-Phe-Gln-Glu-Ile-Val X OH) of the 59-amino acid peptide was found to stimulate the release of gonadotropic hormones from human and baboon anterior pituitary cells in culture. The peptide did not affect thyrotropin or prolactin secretion. A GnRH antagonist did not inhibit gonadotropin stimulation by the peptide, and the peptide did not compete with GnRH for GnRH pituitary receptors, indicating that the action of the peptide is independent of the GnRH receptor. The GnRH precursor contains two distinct peptide sequences capable of stimulating gonadotropin release from human and baboon pituitary cells.

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Naor, Zvi, Henry N. Jabbour, Michal Naidich, Adam J. Pawson, Kevin Morgan, Sharon Battersby, Michael R. Millar, Pamela Brown i Robert P. Millar. "Reciprocal Cross Talk between Gonadotropin-Releasing Hormone (GnRH) and Prostaglandin Receptors Regulates GnRH Receptor Expression and Differential Gonadotropin Secretion". Molecular Endocrinology 21, nr 2 (1.02.2007): 524–37. http://dx.doi.org/10.1210/me.2006-0253.

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Abstract The asynchronous secretion of gonadotrope LH and FSH under the control of GnRH is crucial for ovarian cyclicity but the underlying mechanism is not fully resolved. Because prostaglandins (PG) are autocrine regulators in many tissues, we determined whether they have this role in gonadotropes. We first demonstrated that GnRH stimulates PG synthesis by induction of cyclooxygenase-2, via the protein kinase C/c-Src/phosphatidylinositol 3′-kinase/MAPK pathway in the LβT2 gonadotrope cell line. We then demonstrated that PGF2α and PGI2, but not PGE2 inhibited GnRH receptor expression by inhibition of phosphoinositide turnover. PGF2α, but not PGI2 or PGE2, reduced GnRH-induction of LHβ gene expression, but not the α-gonadotropin subunit or the FSHβ subunit genes. The prostanoid receptors EP1, EP2, FP, and IP were expressed in rat gonadotropes. Incubations of rat pituitaries with PGF2α, but not PGI2 or PGE2, inhibited GnRH-induced LH secretion, whereas the cyclooxygenase inhibitor, indomethacin, stimulated GnRH-induced LH secretion. None of these treatments had any effect on GnRH-induced FSH secretion. The findings have thus elaborated a novel GnRH signaling pathway mediated by PGF2α-FP and PGI2-IP, which acts through an autocrine/paracrine modality to limit autoregulation of the GnRH receptor and differentially inhibit LH and FSH release. These findings provide a mechanism for asynchronous LH and FSH secretions and suggest the use of combination therapies of GnRH and prostanoid analogs to treat infertility, diseases with unbalanced LH and FSH secretion and in hormone-dependent diseases such as prostatic cancer.

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Ukrainets, Roman V., i Yulia S. Korneva. "Endometrial cell apoptosis impairment associated with hormonal imbalance as a key factor in the development of endometriosis". Problems of Endocrinology 65, nr 2 (30.06.2019): 140–44. http://dx.doi.org/10.14341/probl9983.

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The review describes the effect of certain hormones and their imbalance on apoptosis of retrogradely refluxed endometrial cells in the abdominal cavity and the effects of estrogen, progesterone, anti-Mullerian hormone, and gonadotropin-releasing hormone on the internal and external apoptotic pathways of various cell populations in endometriotic foci. The nuclear estrogen receptor (ER-) is shown to inhibit TNF receptors that trigger the external apoptotic pathway, but the effects of estrogens do not play a key role in the pathogenesis of endometriosis. The role of progesterone and changes in the receptor status towards prevalence of PR-A with a decreased response of endometrial tissue to progesterone and inhibition of apoptosis are described. We discuss the role of the anti-Mllerian hormone and gonadotropin-releasing hormone II (GnRH II) as activators of apoptosis in normal endometrial tissue and in endometriosis. Investigation of endocrine effects on apoptosis of parenchymal and stromal cells of endometriotic foci may provide a theoretical basis for searching for new therapeutic targets in this hormone-dependent pathology.

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Krsmanovic, Lazar Z., Antonio J. Martinez-Fuentes, Krishan K. Arora, Nadia Mores, Carlos E. Navarro, Hao-Chia Chen, Stanko S. Stojilkovic i Kevin J. Catt. "Autocrine Regulation of Gonadotropin-Releasing Hormone Secretion in Cultured Hypothalamic Neurons". Endocrinology 140, nr 3 (1.03.1999): 1423–31. http://dx.doi.org/10.1210/endo.140.3.6588.

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Abstract Episodic hormone secretion is a characteristic feature of the hypothalamo-pituitary-gonadal system, in which the profile of gonadotropin release from pituitary gonadotrophs reflects the pulsatile secretory activity of GnRH-producing neurons in the hypothalamus. Pulsatile release of GnRH is also evident in vitro during perifusion of immortalized GnRH neurons (GT1–7 cells) and cultured fetal hypothalamic cells, which continue to produce bioactive GnRH for up to 2 months. Such cultures, as well as hypothalamic tissue from adult rats, express GnRH receptors as evidenced by the presence of high-affinity GnRH binding sites and GnRH receptor transcripts. Furthermore, individual GnRH neurons coexpress GnRH and GnRH receptors as revealed by double immunostaining of hypothalamic cultures. In static cultures of hypothalamic neurons and GT1–7 cells, treatment with the GnRH receptor antagonist, [d-pGlu1, d-Phe2, d-Trp3,6]GnRH caused a prominent increase in GnRH release. In perifused hypothalamic cells and GT1–7 cells, treatment with the GnRH receptor agonist, des-Gly10-[d-Ala6]GnRH N-ethylamide, reduced the frequency and increased the amplitude of pulsatile GnRH release, as previously observed in GT1–7 cells. In contrast, exposure to the GnRH antagonist analogs abolished pulsatile secretion and caused a sustained and progressive increase in GnRH release. These findings have demonstrated that GnRH receptors are expressed in hypothalamic GnRH neurons, and that receptor activation is required for pulsatile GnRH release in vitro. The effects of GnRH agonist and antagonist analogs on neuropeptide release are consistent with the operation of an ultrashort-loop autocrine feedback mechanism that exerts both positive and negative actions that are necessary for the integrated control of GnRH secretion from the hypothalamus.

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STOJILKOVIC, STANKO S., JOHN REINHART i KEVIN J. CATT. "Gonadotropin-Releasing Hormone Receptors: Structure and Signal Transduction Pathways". Endocrine Reviews 15, nr 4 (sierpień 1994): 462–99. http://dx.doi.org/10.1210/edrv-15-4-462.

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Caunt, Christopher J., Ann R. Finch, Kathleen R. Sedgley, Lisa Oakley, Louis M. Luttrell i Craig A. McArdle. "Arrestin-mediated ERK Activation by Gonadotropin-releasing Hormone Receptors". Journal of Biological Chemistry 281, nr 5 (28.11.2005): 2701–10. http://dx.doi.org/10.1074/jbc.m507242200.

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Jennes, Lothar, i P. Michael Conn. "Gonadotropin-Releasing Hormone and Its Receptors in Rat Brain". Frontiers in Neuroendocrinology 15, nr 1 (marzec 1994): 51–77. http://dx.doi.org/10.1006/frne.1994.1003.

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Fernald, Russell D. "Gonadotropin-Releasing Hormone Receptors: Where Did They Come From?" Endocrinology 150, nr 6 (czerwiec 2009): 2507–8. http://dx.doi.org/10.1210/en.2009-0475.

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Cheng, Kwai Wa, i Peter CK Leung. "The expression, regulation and signal transduction pathways of the mammalian gonadotropin-releasing hormone receptor". Canadian Journal of Physiology and Pharmacology 78, nr 12 (1.12.2000): 1029–52. http://dx.doi.org/10.1139/y00-096.

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Normal mammalian sexual maturation and reproductive functions require the integration and precise coordination of hormones at the hypothalamic, pituitary, and gonadal levels. Hypothalamic gonadotropin-releasing hormone (GnRH) is a key regulator in this system; after binding to its receptor (GnRHR), it stimulates de novo synthesis and release of gonadotropins in anterior pituitary gonadotropes. Since the isolation of the GnRHR cDNA, the expression of GnRHR mRNA has been detected not only in the pituitary, but also in extrapituitary tissues, including the ovary and placenta. It has been shown that change in GnRHR mRNA is one of the mechanisms for regulating the expression of the GnRHR. To help understand the molecular mechanism(s) involved in transcriptional regulation of the GnRHR gene, the 5' flanking region of the GnRHR gene has recently been isolated. Initial characterization studies have identified several DNA regions in the GnRHR 5' flanking region which are responsible for both basal expression and GnRH-mediated homologous regulation of this gene in pituitary cells. The mammalian GnRHR lacks a C-terminus and possesses a relatively short third intracellular loop; both features are important in desensitization of many others G-protein coupled receptors (GPCRs), Homologous desensitization of GnRHR has been shown to be regulated by various serine-threonine protein kinases including protein kinase A (PKA) and protein kinase C (PKC), as well as by G-protein coupled receptor kinases (GRKs). Furthermore, GnRHR was demonstrated to couple with multiple G proteins (Gq/11, Gs, and Gi), and to activate cascades that involved the PKC, PKA, and mitogen-activator protein kinases. These results suggest the diversity of GnRHR-G protein coupling and signal transduction systems. The identification of second form of GnRH (GnRH-II) in mammals adds to the complexity of the GnRH-GnRHR system. This review summaries our recent progress in understanding the regulation of GnRHR gene expression and the GnRHR signal transduction pathways.Key words: gonadotropin-releasing hormone receptor, transcriptional regulation, desensitization, signal transduction.

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Rebers, Frank E. M., Peter T. Bosma, Wytske van Dijk, Henk J. T. Goos i Rüdiger W. Schulz. "GnRH stimulates LH release directly via inositol phosphate and indirectly via cAMP in African catfish". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, nr 6 (1.06.2000): R1572—R1578. http://dx.doi.org/10.1152/ajpregu.2000.278.6.r1572.

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In African catfish, two gonadotropin-releasing hormone (GnRH) peptides have been identified: chicken GnRH (cGnRH)-II and catfish GnRH (cfGnRH). The GnRH receptors on pituitary cells producing gonadotropic hormone signal through inositol phosphate (IP) elevation followed by increases in intracellular calcium concentration ([Ca2+]i). In primary pituitary cell cultures of male African catfish, both cGnRH-II and cfGnRH dose dependently elevated IP accumulation, [Ca2+]i, and the release of the luteinizing hormone (LH)-like gonadotropin. In all cases, cGnRH-II was more potent than cfGnRH. The GnRH-stimulated LH release was not associated with elevated cAMP levels, and forskolin-induced cAMP elevation had no effect on LH release. With the use of pituitary tissue fragments, however, cAMP was elevated by GnRH, and forskolin was able to stimulate LH secretion. Incubating these fragments with antibodies against cfGnRH abolished the forskolin-induced LH release but did not compromise the forskolin-induced cAMP elevation. This suggests that cfGnRH-containing nerve terminals are present in pituitary tissue fragments and release cfGnRH via cAMP signaling on GnRH stimulation, whereas the GnRH receptors on gonadotrophs use IP/[Ca2+]i to stimulate the release of LH.

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Peng, Chun, i Spencer T. Mukai. "Activins and their receptors in female reproduction". Biochemistry and Cell Biology 78, nr 3 (2.04.2000): 261–79. http://dx.doi.org/10.1139/o00-007.

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Activins are growth and differentiation factors belonging to the transforming growth factor-β superfamily. They are dimeric proteins consisting of two inhibin β subunits. The structure of activins is highly conserved during vertebrate evolution. Activins signal through type I and type II receptor proteins, both of which are serine/threonine kinases. Subsequently, downstream signals such as Smad proteins are phosphorylated. Activins and their receptors are present in many tissues of mammals and lower vertebrates where they function as autocrine and (or) paracrine regulators of a variety of physiological processes, including reproduction. In the hypothalamus, activins are thought to stimulate the release of gonadotropin-releasing hormone. In the pituitary, activins increase follicle-stimulating hormone secretion and up-regulate gonadotropin-releasing hormone receptor expression. In the ovaries of vertebrates, activins are expressed predominantly in the follicular layer of the oocyte where they regulate processes such as folliculogenesis, steroid hormone production, and oocyte maturation. During pregnancy, activin-A is also involved in the regulation of placental functions. This review provides a brief overview of activins and their receptors, including their structures, expression, and functions in the female reproductive axis as well as in the placenta. Special effort is made to compare activins and their receptors in different vertebrates. Key words: activins, activin receptors, reproductive axis, placenta.

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Zheng, H., J. J. Kavanagh, W. Hu, Q. Liao i S. Fu. "Hormonal therapy in ovarian cancer". International Journal of Gynecologic Cancer 17, nr 2 (2007): 325–38. http://dx.doi.org/10.1111/j.1525-1438.2006.00749.x.

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Ovarian carcinoma continues to be the leading cause of death due to gynecological malignancy. Epidemiologic studies indicate that steroid hormones play roles in ovarian carcinogenesis. Gonadotropins, estrogen, and androgen may be causative factors, while gonadotropin-releasing hormone and progesterone may be protective factors in ovarian cancer pathogenesis. Experimental studies have shown that hormonal receptors are expressed in ovarian cancer cells and mediate the growth-stimulatory or growth-inhibitory effects of the hormones on these cells. Hormonal therapeutic agents have been evaluated in several clinical trials. Most of these trials were conducted in patients with recurrent or refractory ovarian cancer, with modest efficacy and few side effects. Better understanding of the mechanisms through which hormones affect cell growth may improve the efficacy of hormonal therapy. Molecular markers that can reliably predict major clinical outcomes should be investigated further in well-designed trials

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Tiwary, Basant K. "Correlated Evolution of Gonadotropin-Releasing Hormone and Gonadotropin-Inhibitory Hormone and Their Receptors in Mammals". Neuroendocrinology 97, nr 3 (17.10.2012): 242–51. http://dx.doi.org/10.1159/000342694.

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Pawson, Adam J., Elena Faccenda, Stuart Maudsley, Zhi-Liang Lu, Zvi Naor i Robert P. Millar. "Mammalian Type I Gonadotropin-Releasing Hormone Receptors Undergo Slow, Constitutive, Agonist-Independent Internalization". Endocrinology 149, nr 3 (26.11.2007): 1415–22. http://dx.doi.org/10.1210/en.2007-1159.

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Regulatory elements present in the cytoplasmic carboxyl-terminal tails of G protein-coupled receptors contribute to agonist-dependent receptor desensitization, internalization, and association with accessory proteins such as β-arrestin. The mammalian type I GnRH receptors are unique among the rhodopsin-like G protein-coupled receptors because they lack a cytoplasmic carboxyl-terminal tail. In addition, they do not recruit β-arrestin, nor do they undergo rapid desensitization. By measuring the internalization of labeled GnRH agonists, previous studies have reported that mammalian type I GnRH receptors undergo slow agonist-dependent internalization. In the present study, we have measured the internalization of epitope-tagged GnRH receptors, both in the absence and presence of GnRH stimulation. We demonstrate that mammalian type I GnRH receptors exhibit a low level of constitutive agonist-independent internalization. Stimulation with GnRH agonist did not significantly enhance the level of receptor internalization above the constitutive level. In contrast, the catfish GnRH and rat TRH receptors, which have cytoplasmic carboxyl-terminal tails, displayed similar levels of constitutive agonist-independent internalization but underwent robust agonist-dependent internalization, as did chimeras of the mammalian type I GnRH receptor with the cytoplasmic carboxyl-terminal tails of the catfish GnRH receptor or the rat TRH receptor. When the carboxyl-terminal Tyr325 and Leu328 residues of the mammalian type I GnRH receptor were replaced with alanines, these two mutant receptors underwent significantly impaired internalization, suggesting a function for the Tyr-X-X-Leu sequence in mediating the constitutive agonist-independent internalization of mammalian type I GnRH receptors. These findings provide further support for the underlying notion that the absence of the cytoplasmic carboxyl-terminal tail of the mammalian type I GnRH receptors has been selected for during evolution to prevent rapid receptor desensitization and internalization to allow protracted GnRH signaling in mammals.

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Pineda, R., D. Garcia-Galiano, M. A. Sanchez-Garrido, M. Romero, F. Ruiz-Pino, E. Aguilar, F. A. Dijcks i in. "Characterization of the Potent Gonadotropin-Releasing Activity of RF9, a Selective Antagonist of RF-Amide-Related Peptides and Neuropeptide FF Receptors: Physiological and Pharmacological Implications". Endocrinology 151, nr 4 (16.02.2010): 1902–13. http://dx.doi.org/10.1210/en.2009-1259.

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Identification of RF-amide-related peptides (RFRP), as putative mammalian orthologs of the avian gonadotropin-inhibitory hormone, has drawn considerable interest on its potential effects and mechanisms of action in the control of gonadotropin secretion in higher vertebrates. Yet, these analyses have so far relied mostly on indirect approaches, while direct assessment of their physiological roles has been hampered by the lack of suitable antagonists. RF9 was recently reported as a selective and potent antagonist of the receptors for RFRP (RFRPR) and the related neuropeptides, neuropeptide FF (NPFF) and neuropeptide AF (NPFF receptor). We show here that RF9 possesses very strong gonadotropin-releasing activities in vivo. Central administration of RF9 evoked a dose-dependent increase of LH and FSH levels in adult male and female rats. Similarly, male and female mice responded to intracerebroventricular injection of RF9 with robust LH secretory bursts. In rats, administration of RF9 further augmented the gonadotropin-releasing effects of kisspeptin, and its stimulatory effects were detected despite the prevailing suppression of gonadotropin secretion by testosterone or estradiol. In fact, blockade of estrogen receptor-α partially attenuated gonadotropin responses to RF9. Finally, systemic administration of RF9 modestly stimulated LH secretion in vivo, although no direct effects in terms of gonadotropin secretion were detected at the pituitary in vitro. Altogether, these data are the first to disclose the potent gonadotropin-releasing activity of RF9, a selective antagonist of RFRP (and NPFF) receptors. Our findings support a putative role of the RFRP/gonadotropin-inhibitory hormone system in the central control of gonadotropin secretion in mammals and have interesting implications concerning the potential therapeutic indications and pharmacological effects of RF9.

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Amiri, B. Mojazi, Thomas E. Adams, Serge I. Doroshov i Gary P. Moberg. "USE OF MAMMALIAN GONADOTROPIN-RELEASINC HORMONE TO CHARACTERIZE PITUITARY GONADOTROPIN RELEASING HORMONE RECEPTORS IN WHITE STURGEON (Acipenser transtnontanus RICHARDSON)." Journal of Applied Ichthyology 15, nr 4-5 (wrzesień 1999): 318. http://dx.doi.org/10.1111/j.1439-0426.1999.tb00323.x.

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Yu, W. H., S. Karanth, C. A. Mastronardi, S. Sealfon, C. Dean, W. L. Dees i S. M. McCann. "Lamprey GnRH-III Acts on Its Putative Receptor via Nitric Oxide to Release Follicle-Stimulating Hormone Specifically". Experimental Biology and Medicine 227, nr 9 (październik 2002): 786–93. http://dx.doi.org/10.1177/153537020222700910.

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Lamprey gonadotropin-releasing hormone-III (I-GnRH-III), the putative follicle-stimulating hormone (FSH)-releasing factor (FSHRF), exerts a preferential FSH-releasing activity in rats both in vitro and in vivo. To test the hypothesis that I-GnRH-III acts on its own receptors to stimulate gonadotropin release, the functional activity of this peptide at mammalian (m) leutinizing hormone (LH)RH receptors transfected to COS cells was tested. I-GnRH-III activated m-LHRH receptors only at a minimal effective concentration (MEC) of 10–6 M, whereas m-LHRH was active at a MEC of 10–9 M, at least 1,000 times less than that required for I-GnRH-III. In 4-day monolayer cultured cells, I-GnRH-III was similarly extremely weak in releasing either LH or FSH, and, in fact, it released LH at a lower concentration (10–7 M) than that required for FSH release (10–6 M). In this assay, m-LHRH released both FSH and LH significantly at the lowest concentration tested (10–10 M). On the other hand, I-GnRH-III had a high potency to selectively release FSH and not LH from hemipituitaries of male rats. The results suggest that the cultured cells were devoid of FSHRF receptors, thereby resulting in a pattern of FSH and LH release caused by the LHRH receptor. On the other hand, the putative FSH-releasing factor receptor accounts for the selective FSH release by I-GnRH-III when tested on hemipituitaries. Removal of calcium from the medium plus the addition of EGTA, a calcium chelator, suppressed the release of gonadotropins induced by either I-GnRH-III or LHRH, indicating that calcium is required for the action of either peptide. Previous results showed that sodium nitroprusside, a releaser of nitric oxide (NO), causes the release of both FSH and LH from hemipituitaries incubated in vitro. In the present experiments, a competitive inhibitor of NO synthase, L-NG-monomethyl-l-arginine (300 μM) blocked the action of I-GnRH-III or partially purified FSHRF. The results indicate that I-GnRH-III and FSHRF act on putative FSHRF receptors by a calcium-dependent NO pathway.

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29

Harrison, G. S., M. E. Wierman, T. M. Nett i L. M. Glode. "Gonadotropin-releasing hormone and its receptor in normal and malignant cells". Endocrine-Related Cancer 11, nr 4 (grudzień 2004): 725–48. http://dx.doi.org/10.1677/erc.1.00777.

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Gonadotropin-releasing hormone (GnRH) is the hypothalamic factor that mediates reproductive competence. Intermittent GnRH secretion from the hypothalamus acts upon its receptor in the anterior pituitary to regulate the production and release of the gonadotropins, LH and FSH. LH and FSH then stimulate sex steroid hormone synthesis and gametogenesis in the gonads to ensure reproductive competence. The pituitary requires pulsatile stimulation by GnRH to synthesize and release the gonadotropins LH and FSH. Clinically, native GnRH is used in a pump delivery system to create an episodic delivery pattern to restore hormonal defects in patients with hypogonadotropic hypogonadism. Agonists of GnRH are delivered in a continuous mode to turn off reproductive function by inhibiting gonadotropin production, thus lowering sex steroid production, resulting in medical castration. They have been used in endocrine disorders such as precocious puberty, endometriosis and leiomyomata, but are also studied extensively in hormone-dependent malignancies. The detection of GnRH and its receptor in other tissues, including the breast, ovary, endometrium, placenta and prostate suggested that GnRH agonists and antagonists may also have direct actions at peripheral targets. This paper reviews the current data concerning differential control of GnRH and GnRH receptor expression and signaling in the hypothalamic–pituitary axis and extrapituitary tissues. Using these data as a backdrop, we then review the literature about the action of GnRH in cancer cells, the utility of GnRH analogs in various malignancies and then update the research in novel therapies targeted to the GnRH receptor in cancer cells to promote anti-proliferative effects and control of tumor burden.

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30

Ping, Lin, Virendra B. Mahesh, Ganapathy K. Bhat i Darrell W. Brann. "Regulation of Gonadotropin-Releasing Hormone and Luteinizing Hormone Secretion by AMPA Receptors". Neuroendocrinology 66, nr 4 (1997): 246–53. http://dx.doi.org/10.1159/000127245.

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Braden, T. D. "Activin-A stimulates the synthesis of gonadotropin-releasing hormone receptors". Endocrinology 130, nr 4 (1.04.1992): 2101–5. http://dx.doi.org/10.1210/en.130.4.2101.

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Szabó, Janos, Attila Végh, Gergő Rácz i Béla Szende. "Immunohistochemical demonstration of gonadotropin-releasing hormone receptors in prostate carcinoma". Urologic Oncology: Seminars and Original Investigations 23, nr 6 (listopad 2005): 399–401. http://dx.doi.org/10.1016/j.urolonc.2005.04.001.

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Dekel, Nava, Orly Lewysohn, Dan Ayalon i Eli Hazum. "RECEPTORS FOR GONADOTROPIN RELEASING HORMONE ARE PRESENT IN RAT OOCYTES". Endocrinology 123, nr 2 (sierpień 1988): 1205–7. http://dx.doi.org/10.1210/endo-123-2-1205.

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Herbison, Allan E., i Jean-Rémi Pape. "New Evidence for Estrogen Receptors in Gonadotropin-Releasing Hormone Neurons". Frontiers in Neuroendocrinology 22, nr 4 (październik 2001): 292–308. http://dx.doi.org/10.1006/frne.2001.0219.

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Au, Teresa M., Anna K. Greenwood i Russell D. Fernald. "Differential social regulation of two pituitary gonadotropin-releasing hormone receptors". Behavioural Brain Research 170, nr 2 (czerwiec 2006): 342–46. http://dx.doi.org/10.1016/j.bbr.2006.02.027.

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Braden, T. D., i P. M. Conn. "Activin-A stimulates the synthesis of gonadotropin-releasing hormone receptors." Endocrinology 130, nr 4 (kwiecień 1992): 2101–5. http://dx.doi.org/10.1210/endo.130.4.1312442.

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Behrman, Harold R., Raymond F. Aten i Yael Margolin. "Gonadotropin-releasing hormone binding inhibitors in the ovary". Canadian Journal of Physiology and Pharmacology 67, nr 8 (1.08.1989): 954–56. http://dx.doi.org/10.1139/y89-150.

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A protein present in ovaries and other tissues of many species competitively and reversibly inhibits high affinity binding of gonadotropin-releasing hormone (GnRH) to rat ovarian membranes, but this protein is not GnRH. This protein has been partially purified and characterized from bovine ovaries. The absence of GnRH binding inhibitory (GBI) activity in plasma and follicular fluid indicates that this protein may act in a localized manner within or near its site of production or release. The bovine ovarian GBI protein evokes antigonadotropic activity in ovarian cells from both the rat and the bovine. The biological effect of GBI may occur independently of interaction with high affinity binding sites for GnRH, since these are absent from the bovine ovary. Thus, the GBI protein may abrogate gonadotropin-dependent responses in ovarian cells by mechanisms separate from interaction with GnRH receptors. A complete characterization of the GBI protein and evaluation of its mechanism of action in ovarian and pituitary cells will dictate conclusions on the physiological importance of this protein.Key words: gonadotropin-releasing hormone, luteinizing hormone, follicle-stimulating hormone, granulosa cells, luteal cells, ovary.

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Thackray, Varykina G., Jennifer L. Hunnicutt, Aisha K. Memon, Yasmin Ghochani i Pamela L. Mellon. "Progesterone Inhibits Basal and Gonadotropin-Releasing Hormone Induction of Luteinizing Hormone β-Subunit Gene Expression". Endocrinology 150, nr 5 (23.12.2008): 2395–403. http://dx.doi.org/10.1210/en.2008-1027.

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LH and FSH play critical roles in mammalian reproduction by mediating steroidogenesis and gametogenesis in the gonad. Gonadal steroid hormone feedback to the hypothalamus and pituitary influences production of the gonadotropins. We previously demonstrated that progesterone differentially regulates the expression of the LH and FSH β-subunits at the level of the gonadotrope: FSHβ transcription is induced, whereas LHβ is repressed. In this study, we investigated the mechanism of progesterone repression of LHβ gene expression using immortalized gonadotrope-derived LβT2 cells. The progesterone suppression of both basal and GnRH-induced LHβ gene expression occurs in a hormone- and receptor-dependent manner. Chromatin immunoprecipitation demonstrates that the hormone-bound progesterone receptor (PR) is recruited to the endogenous mouse LHβ promoter. In addition, suppression requires both the amino-terminal and DNA-binding regions of PR. Furthermore, progesterone suppression does not require direct PR binding to the promoter, and, thus, PR is likely recruited to the promoter via indirect binding through other transcription factors. These data demonstrate that the molecular mechanism for progesterone action on the LHβ promoter is distinct from FSHβ, which involves direct PR binding to the promoter to produce activation. It also differs from androgen repression of LHβ gene expression in that, rather than Sp1 or steroidogenic factor-1 elements, it requires elements within −300/−250 and −200/−150 that also contribute to basal expression of the LHβ promoter. Altogether, our data indicate that progesterone feedback at the level of the pituitary gonadotrope is likely to play a key role in differential production of the gonadotropin genes.

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Hasan AL-Mutar, Hayder Abdul-Kareem. "Investigation the polymorphism of gonadotropin releasing hormone receptor gene in Iraq sheep". Iraqi Journal of Veterinary Medicine 41, nr 1 (5.06.2017): 138–44. http://dx.doi.org/10.30539/iraqijvm.v41i1.96.

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In the present study, the investigation includes the estrus activity after synchronization of estrus by using 20 mg impregnated sponges with Medroxy Progesterone Acetate for 12 days with 400 IU I/M injection of pregnant mare serum gonadotropin 24 hrs. before sponges withdrawal. All 30 Iraqi sheep's showed (100%) estrus after sponge withdrawal. Twin percentage 40% while single percentage 60%. The polymorphisms of gonadotropin-releasing hormone receptor gene were analyzed as a genetic marker in 30 Iraqi sheep's. Two noticed genotypes (GA and GT), and single nucleotide polymorphisms in the exon2 region of gonadotropin-releasing hormone receptor gene as genetic marker and correlated with high litter size after hormonal super ovulation response in sheep. The frequencies of alleles G,A and G,T in Iraqi ovine breeds were 0.50 and 0.50, respectively the outcomes revealed that GA, GT genotype was related with better litter-size in Iraqi ovine breeds. Therefore, these outcomes recommend that gonadotropin-releasing hormone receptor gene is a powerful candidate gene that impacts litter-size in sheep.

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Salisbury, Travis B., April K. Binder i John H. Nilson. "Welcoming β-Catenin to the Gonadotropin-Releasing Hormone Transcriptional Network in Gonadotropes". Molecular Endocrinology 22, nr 6 (1.06.2008): 1295–303. http://dx.doi.org/10.1210/me.2007-0515.

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Abstract GnRH binds its G-coupled protein receptor, GnRHR, on pituitary gonadotropes and stimulates transcription of Cga, Lhb, and Fshb. These three genes encode two heterodimeric glycoprotein hormones, LH and FSH, that act as gonadotropins by regulating gametogenesis and steroidogenesis in both the testes and ovary. GnRH also regulates transcription of Gnrhr. Thus, regulated expression of Cga, Lhb, Fshb, and Gnrhr provides a genomic signature unique to functional gonadotropes. Steadily increasing evidence now indicates that GnRH regulates transcription of its four signature genes indirectly through a hierarchical transcriptional network that includes distinct subclasses of DNA-binding proteins that comprise the immediate early gene (IEG) family. These IEGs, in turn, confer hormonal responsiveness to the four signature genes. Although the IEGs confer responsiveness to GnRH, they cannot act alone. Instead, additional DNA-binding proteins, including the orphan nuclear receptor steroidogenic factor 1, act permissively to allow the four signature genes to respond to GnRH-induced changes in IEG levels. Emerging new findings now indicate that β-catenin, a transcriptional coactivator and member of the canonical WNT signaling pathway, also plays an essential role in transducing the GnRH signal by interacting with multiple DNA-binding proteins in gonadotropes. Herein we propose that these interactions with β-catenin define a multicomponent transcriptional network required for regulated expression of the four signature genes of the gonadotrope, Cga, Lhb, Fshb, and Gnrhr.

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Bedoukian, Matthew A., Jennifer D. Whitesell, Erik J. Peterson, Colin M. Clay i Kathryn M. Partin. "The Stargazin C Terminus Encodes an Intrinsic and Transferable Membrane Sorting Signal". Journal of Biological Chemistry 283, nr 3 (6.11.2007): 1597–600. http://dx.doi.org/10.1074/jbc.m708141200.

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Activity-dependent plasticity of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors is regulated by their auxiliary subunit, stargazin. Association with stargazin enhances α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor surface expression and modifies the receptor's biophysical properties. Fusing the cytoplasmic C terminus of stargazin to the C-terminal domains of either GluR1 or the gonadotropin-releasing hormone receptor permits efficient trafficking from the endoplasmic reticulum and sorting to the basolateral membrane without altering other properties of either receptor.

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Nakane, Ryo, i Yoshitaka Oka. "Excitatory Action of GABA in the Terminal Nerve Gonadotropin-Releasing Hormone Neurons". Journal of Neurophysiology 103, nr 3 (marzec 2010): 1375–84. http://dx.doi.org/10.1152/jn.00910.2009.

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The terminal nerve (TN)-gonadotropin-releasing hormone (GnRH) neurons have been suggested to function as a neuromodulatory system that regulates the motivational and arousal state of the animal and have served as a model system for the study of GnRH neuron physiology. To investigate the synaptic control of the TN-GnRH neurons, we analyzed electrophysiologically the effect of GABA on the TN-GnRH neurons. GABA generally hyperpolarizes most of the neurons in the adult brain by activating GABAA receptors while the activation of GABAA receptors depolarizes some specific neurons in the mature brain. Here we examined the GABAA receptor-mediated responses in the TN-GnRH neurons of adult teleost fish, the dwarf gourami, by means of gramicidin-perforated patch-clamp and cell-attached patch-clamp recordings. The reversal potential for the currents through GABAA receptors under the voltage clamp was depolarized relative to the resting membrane potential. GABAA receptor activation depolarized TN-GnRH neurons under the current clamp and had excitatory effect on their electrical activity, whereas the stronger GABAA receptor activation had bidirectional effect (excitatory–inhibitory). This excitatory effect is suggested to arise from high [Cl−]i and was shown to be suppressed by bumetanide, the blocker of Cl−-accumulating sodium-potassium-2-chloride co-transporter (NKCC). The present results demonstrate that GABAA receptor activation induces excitation in TN-GnRH neurons, which may facilitate their neuromodulatory functions by increasing their spontaneous firing frequencies. The excitatory actions of GABA in the adult brain have recently been attracting much attention, and the easily accessible large TN-GnRH neurons should be a nice model system to analyze their physiological functions.

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Menon, M., H. Peegel i V. Katta. "Estradiol potentiation of gonadotropin-releasing hormone responsiveness in the anterior pituitary is mediated by an increase in gonadotropin-releasing hormone receptors". American Journal of Obstetrics and Gynecology 151, nr 4 (luty 1985): 534–40. http://dx.doi.org/10.1016/0002-9378(85)90284-4.

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Singh, R., T. Pretheeban i R. Rajamahendran. "GnRH agonist (buserelin) up regulates estrogen receptor α mRNA but not estrogen receptor β and progesterone receptor mRNA in bovine endometrium in vitro". Canadian Journal of Animal Science 89, nr 4 (1.12.2009): 467–73. http://dx.doi.org/10.4141/cjas08120.

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The local modulatory role of gonadotropin releasing hormone (GnRH), gonadotropin releasing hormone receptor (GnRH-R) system in regulating steroid hormone receptors at the endometrial level is still not known. Estrogen and progesterone maintain uterine functions by acting through their corresponding receptors; estrogen receptors (ERα and ERβ) and progesterone receptors (PR). We recently demonstrated GnRH-R in bovine endometrium and find the co-existence of GnRH and steroid hormone receptors in endometrium as interesting. Our objective was to determine the effect of a GnRH agonist (buserelin), on the expression of ERα, ERβ, and PR messenger RNA (mRNA) in bovine endometrium. Reproductive tracts were collected from slaughtered cows at a local abattoir, and endometrial explants were treated with buserelin (0, 200, 500, 1000 ng mL-1 respectively), GnRH antagonist-antide (500 ng mL-1) and antide + buserelin (500+200 ng mL-1) for 6 h and stored at -80°C for RNA extraction. Two micrograms of total RNA was subjected to reverse transcription polymerase chain reaction, PCR products electrophoresed (2% agrose gel); visualized and statistically analyzed. The results showed that buserelin (200 ng mL-1) increased the expression of ERα in the luteal phase endometrium. In addition, the expression of endometrial ERα was greater during the follicular than luteal phase. This up regulation of ERα mRNA in luteal phase endometrium suggests that GnRH administration may influence pregnancy in bovines. Key words: GnRH, bovine, endometrium, estrogen receptors, progesterone receptors

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Roberts, Stanley A., Terry M. Nett, Howard A. Hartman, Thomas E. Adams i Raymond E. Stoll. "SDZ 200–110 Induces Leydig Cell Tumors By Increasing Gonadotropins in Rats". Journal of the American College of Toxicology 8, nr 3 (maj 1989): 487–505. http://dx.doi.org/10.3109/10915818909014534.

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The administration of 62.5 mg/kg/day of SDZ 200–110, a calcium channel blocker, for 2 years increased the incidence of Leydig cell tumors while decreasing pituitary tumors in Sprague-Dawley rats. Lower doses did not change the incidence of these tumors. No other endocrine tumors were seen in rats or mice of either sex. A single gavage dose of 62.5 mg/kg/day decreased serum testosterone levels by 90% 4 hr after dosing. In vitro testosterone production by Leydig cells from these animals was minimally decreased, which suggests that a direct inhibition of steroid synthesis was removed during cell isolation. Dietary administration of the drug for 10 weeks did not significantly alter levels of serum hormones or testicular luteinizing hormone (LH) and gonadotropin-releasing hormone (GnRH) receptors, although a significant elevation of testicular testosterone levels was seen. Increased serum levels of LH and follicle-stimulating hormone (FSH) were seen after 52 and 66 weeks, respectively, of dietary feeding of 62.5 mg/kg/day. The increase in serum LH was observed to week 104, while FSH levels returned to control levels by week 94. No effect on gonadotropin receptors was seen at the 6.25 mg/kg/day dosage. The age-related increase in serum prolactin was markedly reduced by 62.5 mg/kg/day of SDZ 200–110 in weeks 66 to 104 and to a lesser extent at the 6.25 mg/kg/day dosage. Testicular LH receptors were decreased by the high dose in animals sacrificed after 90–104 weeks. In conclusion, SDZ 200–110 increases the incidence of Leydig cell tumors by elevating levels of serum gonadotropins. The suggested mechanism for this increase in gonadotropins is a result of the effects of SDZ 200–110 on serum hormones and testicular LH receptors. The drug was judged not to pose a risk to humans since no change in gonadotropin levels was observed after chronic treatment.

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Tzoupis, Haralambos, Agathi Nteli, Maria-Eleni Androutsou i Theodore Tselios. "Gonadotropin-Releasing Hormone and GnRH Receptor: Structure, Function and Drug Development". Current Medicinal Chemistry 27, nr 36 (4.11.2020): 6136–58. http://dx.doi.org/10.2174/0929867326666190712165444.

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Background: Gonadotropin-Releasing Hormone (GnRH) is a key element in sexual maturation and regulation of the reproductive cycle in the human organism. GnRH interacts with the pituitary cells through the activation of the Gonadotropin Releasing Hormone Receptors (GnRHR). Any impairments/dysfunctions of the GnRH-GnRHR complex lead to the development of various cancer types and disorders. Furthermore, the identification of GnRHR as a potential drug target has led to the development of agonist and antagonist molecules implemented in various treatment protocols. The development of these drugs was based on the information derived from the functional studies of GnRH and GnRHR. Objective: This review aims at shedding light on the versatile function of GnRH and GnRH receptor and offers an apprehensive summary regarding the development of different agonists, antagonists and non-peptide GnRH analogues. Conclusion: The information derived from these studies can enhance our understanding of the GnRH-GnRHR versatile nature and offer valuable insight into the design of new more potent molecules.

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Bhattarai, Janardhan P., Seon Ah Park, Jin Bong Park, So Yeong Lee, Allan E. Herbison, Pan Dong Ryu i Seong Kyu Han. "Tonic Extrasynaptic GABAA Receptor Currents Control Gonadotropin-Releasing Hormone Neuron Excitability in the Mouse". Endocrinology 152, nr 4 (1.02.2011): 1551–61. http://dx.doi.org/10.1210/en.2010-1191.

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Abstract It is well established that the GABAA receptor plays an important role in regulating the electrical excitability of GnRH neurons. Two different modes of GABAA receptor signaling exist: one mediated by synaptic receptors generating fast (phasic) postsynaptic currents and the other mediated by extrasynaptic receptors generating a persistent (tonic) current. Using GABAA receptor antagonists picrotoxin, bicuculline methiodide, and gabazine, which differentiate between phasic and tonic signaling, we found that ∼50% of GnRH neurons exhibit an approximately 15-pA tonic GABAA receptor current in the acute brain slice preparation. The blockade of either neuronal (NO711) or glial (SNAP-5114) GABA transporter activity within the brain slice revealed the presence of tonic GABA signaling in ∼90% of GnRH neurons. The GABAA receptor δ subunit is only found in extrasynaptic GABAA receptors. Using single-cell RT-PCR, GABAA receptor δ subunit mRNA was identified in GnRH neurons and the δ subunit–specific agonist 4,5,6,7-tetrahydroisoxazolo [5,4-c] pyridin-3-ol was found to activate inward currents in GnRH neurons. Perforated-patch clamp studies showed that 4,5,6,7-tetrahydroisoxazolo [5,4-c] pyridin-3-ol exerted the same depolarizing or hyperpolarizing effects as GABA on juvenile and adult GnRH neurons and that tonic GABAA receptor signaling regulates resting membrane potential. Together, these studies reveal the presence of a tonic GABAA receptor current in GnRH neurons that controls their excitability. The level of tonic current is dependent, in part, on neuronal and glial GABA transporter activity and mediated by extrasynaptic δ subunit–containing GABAA receptors.

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Brito, Vinicius Nahime, Ana Claudia Latronico, Ivo J. P. Arnhold i Berenice Bilharinho Mendonça. "Update on the etiology, diagnosis and therapeutic management of sexual precocity". Arquivos Brasileiros de Endocrinologia & Metabologia 52, nr 1 (luty 2008): 18–31. http://dx.doi.org/10.1590/s0004-27302008000100005.

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Precocious puberty is defined as the development of secondary sexual characteristics before the age of 8 years in girls and 9 years in boys. Gonadotropin-dependent precocious puberty (GDPP) results from the premature activation of the hypothalamic-pituitary-gonadal axis and mimics the physiological pubertal development, although at an inadequate chronological age. Hormonal evaluation, mainly through basal and GnRH-stimulated LH levels shows activation of the gonadotropic axis. Gonadotropin-independent precocious puberty (GIPP) is the result of the secretion of sex steroids, independently from the activation of the gonadotropic axis. Several genetic causes, including constitutive activating mutations in the human LH-receptor gene and activating mutations in the Gs protein a-subunit gene are described as the etiology of testotoxicosis and McCune-Albright syndrome, respectively. The differential diagnosis between GDPP and GIPP has direct implications on the therapeutic option. Long-acting gonadotropin-releasing hormone (GnRH) analogs are the treatment of choice in GDPP. The treatment monitoring is carried out by clinical examination, hormonal evaluation measurements and image studies. For treatment of GIPP, drugs that act by blocking the action of sex steroids on their specific receptors (cyproterone, tamoxifen) or through their synthesis (ketoconazole, medroxyprogesterone, aromatase inhibitors) are used. In addition, variants of the normal pubertal development include isolated forms of precocious thelarche, precocious pubarche and precocious menarche. Here, we provide an update on the etiology, diagnosis and management of sexual precocity.

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Piva, Flavio, Margherita Piccolella, Elio Messi, Marek Demissie, Anna Cariboni, Savino Selleri, Athina Samara, Giuseppe Gonsalez i Robero Maggi. "Role of glucocorticoid receptors in mouse neurons secreting gonadotropin releasing hormone". Frontiers in Neuroendocrinology 27, nr 1 (maj 2006): 75. http://dx.doi.org/10.1016/j.yfrne.2006.03.156.

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Hazum, Eli. "Purification of gonadotropin releasing hormone receptors using the avidin—biotin technique". Journal of Chromatography A 510 (czerwiec 1990): 233–38. http://dx.doi.org/10.1016/s0021-9673(01)93757-4.

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