Journal articles on the topic 'Gonadotrophin Hormone Releasing Hormone (GnRH)'
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1
Leaños-Miranda, Alfredo, Alfredo Ulloa-Aguirre, Laura A. Cervini, Jo Ann Janovick, Jean Rivier, and P. Michael Conn. "Identification of new gonadotrophin-releasing hormone partial agonists." Journal of Endocrinology 189, no. 3 (June 2006): 509–17. http://dx.doi.org/10.1677/joe.1.06724.
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GnRH agonists or antagonists are currently utilized as therapeutic agents in a number of diseases. A side-effect of prolonged treatment with GnRH analogues is hypoestrogenism. In this study, we tested the in vitro potency of different GnRH analogues originally found to be partial agonists (i.e. analogues with decreased efficacy for activating or stimulating their cognate receptor) as well as novel analogues, to identify compounds that might potentially be useful for partial blockade of gonadotrophin release. Cultured COS-7 cells transiently expressing the rat or human GnRH receptor (GnRHR) were exposed to increasing concentrations (10−8 to 10−5 M) of GnRH analogues (c(4–10)[Asp4,DNal6,Dpr10]-GnRH; c(4–10) [Dpr4,DNal6,Asp10]-GnRH; c(4–10)[Cys4,10,DNal6]-GnRH; c[Eaca1,DNal6]-GnRH; c[Gly1,DNal6]-GnRH; c[βAla1,DTrp6]-GnRH; c[Dava1,DNal6]-GnRH; c[Gaba1, DNal6]-GnRH), and the ability of these analogues to provoke or antagonize GnRH-stimulated inositol phosphate production was assessed. With both human and rat GnRHRs, c[Eaca1,DNal6]-GnRH, c[Gly1,DNal6]-GnRH, c[βAla1,DTrp6]-GnRH and c[Dava1,DNal6]-GnRH exhibited partial agonist activity (35–87% of the maximal efficacy shown by 10−6 M GnRH), whereas c[Gaba1,DNal6]-GnRH behaved as a partial agonist with the human GnRHR and as full agonist with the rat GnRHR. c(4–10)[Asp4, DNal6,Dpr10]-GnRH and c(4–10)[Dpr4,DNal6,Asp10]-GnRH exhibited full antagonist activity with both GnRHRs, and c(4–10) [Cys4,10,DNal6]-GnRH was a weak, partial agonist with the human GnRHR and a full antagonist with the rat GnRHR. With the exception of c[Gaba1,DNal6]-GnRH stimulation of the human GnRHR, and c[Dava1,DNal6]-GnRH and c[Gaba1, DNal6]-GnRH stimulation of the rat GnRHR, all partial agonists also exhibited antagonist activity in the presence of the exogenous full agonist. The results demonstrate that structurally similar analogues display variable potencies and efficacies in vitro for a specific GnRHR as well as for the human versus the rat GnRHR. Their ultimate in vivo usefulness to treat clinical conditions in which complete suppression of gonadotroph activity is not required remains to be investigated.
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King, J. A., J. S. Davidson, and R. P. Millar. "Interaction of endogenous chicken gonadotrophin-releasing hormone-I and -II on chicken pituitary cells." Journal of Endocrinology 117, no. 1 (April 1988): 43–49. http://dx.doi.org/10.1677/joe.0.1170043.
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ABSTRACT The presence of two endogenous forms of gonadotrophin-releasing hormone (GnRH) in the chicken hypothalamus (chicken GnRH-I ([Gln8]GnRH) and chicken GnRH-II ([His5,Trp7,Tyr8]GnRH)), and the stimulation of gonadotrophins by both forms, suggests the possible existence of GnRH receptor subtypes and gonadotroph subtypes in the chicken pituitary. This question was investigated by assessing the effects of various combinations of the two known forms of chicken hypothalamic GnRH and antagonist analogues of GnRH on LH release from dispersed chicken anterior pituitary cells in both static and perifused systems. The relative inhibition of chicken GnRH-I-stimulated and chicken GnRH-II-stimulated LH release by 12 GnRH antagonists did not differ significantly, suggesting a single GnRH receptor type. Chicken GnRH-II was approximately sixfold more potent than chicken GnRH-I in releasing LH. Release of LH in response to maximal doses of chicken GnRH-I and chicken GnRH-II and to a mixture of both was similar and the two peptides were not additive in their effects, consistent with the presence of a single type of LH gonadotroph and a GnRH receptor which binds both forms of GnRH. Each form of GnRH desensitized cells to subsequent stimulation with the other form, providing additional evidence for a single type of LH gonadotroph. These findings suggest that chicken GnRH-I and -II stimulate gonadotrophin release through a single GnRH receptor type on a single class of LH gonadotroph in the chicken pituitary. J. Endocr. (1988) 117,43–49
3
Wilson, C. A., A. J. Leigh, and A. J. Chapman. "Gonadotrophin glycosylation and function." Journal of Endocrinology 125, no. 1 (April 1990): 3–14. http://dx.doi.org/10.1677/joe.0.1250003.
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ABSTRACT This review emphasizes the heterogeneous structure of the gonadotrophin hormones and the influence of different oligosaccharide structures on the bioactivity of these hormones. A summary has been made of the changes in biopotency of the gonadotrophins throughout the life-cycle of the human and in different endocrine states in the rat. In general it appears that the charge of the gonadotrophin conferred by the acid radicals attached to the terminal groups on the oligosaccharide structures strongly influences biopotency. Basic structures have a greater potency in in-vitro assays, but a short half-life in the circulation, while acidic isoforms are less potent, but have a longer circulatory time and are thus more active in in-vivo estimations. More basic forms are secreted over the adult reproductive years compared with the prepubertal period and old age. The glycosyl structure of the carbohydrate groups also alters in different endocrine states and is probably also important for the bioactivity and potency of the hormone. Gonadotrophin-releasing hormone (GnRH) and gonadal steroids can influence the type of isoform synthesized and released, and therefore affect the function of gonadotrophins. GnRH enhances glycosylation, sulphation and biopotency. Oestradiol potentiates the glycosylation induced by GnRH and reduces sialylation, while testosterone increases sialylation. Journal of Endocrinology (1990) 125, 3–14
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Goto, K., F. Kotsuji, and T. Tominaga. "Divergent effects of gonadotrophin-releasing hormone (GnRH) analogue and authentic GnRH on the anterior pituitary gland of rats with restricted feeding." Journal of Endocrinology 145, no. 3 (June 1995): 501–11. http://dx.doi.org/10.1677/joe.0.1450501.
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Abstract The effects of gonadotrophin-releasing hormone analogue (GnRHa; buserelin) on the pituitary function and morphology of food-restricted rats were compared with those of authentic GnRH. After adult female rats had been restricted to 10 g food/day for 60 days, various doses of GnRHa (10 ng, 100 ng and 1 μg) or GnRH (10 μg) were administered either daily for 7 days or twice a week for 4 weeks from day 61 of the period of underfeeding. Underfeeding brought about a decrease in the pituitary gonadotrophin content, serum levels of gonadotrophins and oestradiol, and the number and size of both LH- and FSH-positive pituitary cells. Daily and/or twice-weekly administration of authentic GnRH to underfed rats produced an increase in pituitary and serum gonadotrophin levels and the number and size of both LH- and FSH-positive pituitary cells. The administration of GnRHa daily for 7 days increased serum gonadotrophin levels, while it produced a reduction in the pituitary gonadotrophin content and number and size of both LH- and FSH-positive pituitary cells in a dose-dependent manner. Twice-weekly administration of GnRHa also produced an elevation of serum gonadotrophin levels and reduction of pituitary gonadotrophin content, although it did not affect the numbers and areas of LH- and FSH-positive pituitary cells. A GnRH loading test performed after the GnRHa treatment showed that the GnRHa treatment performed in this study did not produce down-regulation of the GnRH receptor. Thus, it can be concluded that the gonadotrophin-synthesizing activity of GnRHa is weaker than that of authentic GnRH, or that GnRHa may preferentially exert gonadotrophin-releasing activity rather than gonadotrophin-synthesizing activity in the anterior pituitary of underfed rats. Journal of Endocrinology (1995) 145, 501–511
5
Bosma, P. T., S. M. Kolk, F. E. M. Rebers, O. Lescroart, I. Roelants, P. H. G. M. Willems, and R. W. Schulz. "Gonadotrophs but not somatotrophs carry gonadotrophin-releasing hormone receptors: receptor localisation, intracellular calcium, and gonadotrophin and GH release." Journal of Endocrinology 152, no. 3 (March 1997): 437–46. http://dx.doi.org/10.1677/joe.0.1520437.
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Gonadotrophs are the primary target cells for GnRH in the pituitary. However, during a limited period of neonatal life in the rat, lactotrophs and somatotrophs respond to GnRH as well. Also, in the adults of a number of teleost fishes (e.g. carp, goldfish, and tilapia but not trout), GnRH is a potent GH secretagogue. In studying hypophysiotrophic actions of the two forms of GnRH present in the African catfish (Clarias gariepinus), chicken GnRH-II ([His5,Trp7,Tyr8]GnRH; cGnRH-II) and catfish GnRH ([His5,Asn8]GnRH; cfGnRH), we have investigated the effects of GnRH on catfish gonadotrophs and somatotrophs. GnRH binding was examined by incubating dispersed pituitary cells attached to coverslips with 125I-labelled [d-Arg6,Trp7,Leu8,Pro9-Net]GnRH (sGnRHa), a salmon GnRH analogue with high affinity for the GnRH receptor. Following fixation and immunohistochemistry using antisera against catfish LH and GH, 125I-labelled sGnRHa was localised autoradiographically and silver grains were quantified on gonadotrophs and somatotrophs. Specific binding of 125I-labelled sGnRHa was restricted to gonadotrophs. Both cfGnRH and cGnRH-II dose-dependently inhibited 125I-labelled sGnRHa binding to gonadotrophs. To substantiate the localisation of functional GnRH receptors, the effects of cfGnRH and cGnRH-II on the cytosolic free calcium concentration ([Ca2+]i) were examined in Fura-2-loaded somatotrophs and gonadotrophs. GnRH-induced increases in [Ca2+]i appeared to be confined to gonadotrophs, in which both endogenous GnRHs caused a single and transient increase in [Ca2+]i. The amplitude of this [Ca2+]i transient depended on the GnRH dose and correlated well with the GnRHs' effect on LH release. In vivo experiments demonstrated that GnRH treatments which markedly elevated plasma LH levels had no effect on plasma GH levels, while a dopamine agonist (apomorphine) significantly elevated plasma GH levels. We conclude that the two endogenous forms of GnRH in the African catfish are not directly involved in the regulation of the release of GH, suggesting that GnRHs cannot be considered as GH secretagogues in teleosts in general. Journal of Endocrinology (1997) 152, 437–446
6
Evans, J. J., G. Robinson, and K. J. Catt. "Gonadotrophin-releasing activity of neurohypophysial hormones: I. Potential for modulation of pituitary hormone secretion in rats." Journal of Endocrinology 122, no. 1 (July 1989): 99–106. http://dx.doi.org/10.1677/joe.0.1220099.
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ABSTRACT Neurohypophysial hormones have been implicated in the control of anterior pituitary function, and oxytocin has been shown to stimulate gonadotrophin excretion and ovarian follicular development in certain species. To determine the role of neurohypophysial peptides in the control of gonadotrophin release, their actions on LH and FSH secretion were analysed in rats in vivo and in vitro. In adult female rats, administration of oxytocin during early pro-oestrus advanced the spontaneous LH surge and markedly increased peripheral LH levels at 15.00 h compared with control animals. In cultured pituitary cells from adult female rats, oxytocin and vasopressin elicited dose-related increases in LH and FSH release. Such responses were not affected by a potent gonadotrophin-releasing hormone (GnRH) antagonist that abolished GnRH agonist-induced release of LH and FSH. Oxytocin did not enhance GnRH agonist-stimulated gonadotrophin release to the same extent as it increased basal secretion, but at low concentrations of GnRH agonist the effects were additive. The gonadotrophin responses to oxytocin and vasopressin were inhibited by the specific neurohypophysial hormone antagonists, [d(CH2)5d-Ile2,Ile4,Arg8]vasopressin and [d(CH2)5Tyr (Me),Arg8]vasopressin. These results provide direct evidence that neurohypophysial hormones can stimulate gonadotrophin secretion through a receptor system distinct from the GnRH receptor. Such a mechanism could represent a complementary hypothalamic control system for long-term modulation of LH and FSH secretion by exerting a basal or tonic influence on gonadotrophin production. Journal of Endocrinology (1989) 122, 99–106
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Bonnin, M., M. Mondain-Monval, M. C. Audy, and R. Scholler. "Basal and gonadotropin releasing hormone stimulated gonadotropin levels in the female red fox (Vulpes vulpes L.). Negative feedback of ovarian hormones during anoestrus." Canadian Journal of Zoology 67, no. 3 (March 1, 1989): 759–65. http://dx.doi.org/10.1139/z89-107.
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In the red fox, Vulpes vulpes L., an inhibition of gonadotropic function is observed in early anoestrus, particularly during lactation. During this period, secretion of progesterone as a result of the persistent corpora lutea after parturition and episodic releases of estradiol signify ovarian activity, suggesting involvement of these hormones in the modulation of pituitary hormones (luteinizing hormone (LH), follicle-stimulating hormone (FSH)). Effects of ovariectomy and (or) progesterone or estradiol treatments in vivo upon basal and gonadotropin releasing hormone (GnRH)-stimulated LH and FSH were observed. After ovariectomy, a great increase in the basal level of both gonadotropins and in GnRH-stimulated LH release, but not GnRH-stimulated FSH release, were observed. Progesterone treatment induced a decrease in GnRH-stimulated LH and FSH secretions and a decrease in basal LH and FSH levels in ovariectomized females. Estradiol treatment abolished basal secretions and GnRH responses for both hormones. These results suggest a negative feedback of both ovarian steroids at the hypothalamopituitary level on LH and FSH secretions during early anoestrus.
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Kotsuji, F., K. Hosokawa, and T. Tominaga. "Effects of the daily administration of gonadotrophin-releasing hormone on the anterior pituitary gland of rats with restricted feeding." Journal of Endocrinology 134, no. 2 (August 1992): 177—NP. http://dx.doi.org/10.1677/joe.0.1340177.
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ABSTRACT To investigate the influence of weight reduction on pituitary function and its modulation by gonadotrophin-releasing hormone (GnRH), female rats were restricted to 10 g food/day for 60 days. GnRH (5 μg) or saline (0·2 ml) were administered daily between days 31 and 60 of the period of underfeeding. Underfeeding brought about a decrease in the pituitary gonadotrophin content, serum levels of gonadotrophins and oestradiol, and the number and size of both LH- and FSH-positive pituitary cells. The administration of GnRH to underfed rats produced an increase in the pituitary and serum gonadotrophin levels and the number and size of both LH- and FSH-positive pituitary cells. These observations suggest that underfeeding and/or weight loss diminish the number and activity of the pituitary gonadotrophs, and that daily administration of GnRH both increases the number of gonadotrophs and augments their activity. Journal of Endocrinology (1992) 134, 177–182
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Moncaut, Natalia, Gustavo Somoza, Deborah M. Power, and Adelino V. M. Canário. "Five gonadotrophin-releasing hormone receptors in a teleost fish: isolation, tissue distribution and phylogenetic relationships." Journal of Molecular Endocrinology 34, no. 3 (June 2005): 767–79. http://dx.doi.org/10.1677/jme.1.01757.
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Gonadotrophin-releasing hormone (GnRH) is the main neurohormone controlling gonadotrophin release in all vertebrates, and in teleost fish also of growth hormone and possibly of other adenohypophyseal hormones. Over 20 GnRHs have been identified in vertebrates and protochoordates and shown to bind cognate G-protein couple receptors (GnRHR). We have searched the puffer fish, Fugu rubripes, genome sequencing database, identified five GnRHR genes and proceeded to isolate the corresponding complementary DNAs in European sea bass, Dicentrachus labrax. Phylogenetic analysis clusters the European sea bass, puffer fish and all other vertebrate receptors into two main lineages corresponding to the mammalian type I and II receptors. The fish receptors could be subdivided in two GnRHR1 (A and B) and three GnRHR2 (A, B and C) subtypes. Amino acid sequence identity within receptor subtypes varies between 70 and 90% but only 50–55% among the two main lineages in fish. All European sea bass receptor mRNAs are expressed in the anterior and mid brain, and all but one are expressed in the pituitary gland. There is differential expression of the receptors in peripheral tissues related to reproduction (gonads), chemical senses (eye and olfactory epithelium) and osmoregulation (kidney and gill). This is the first report showing five GnRH receptors in a vertebrate species and the gene expression patterns support the concept that GnRH and GnRHRs play highly diverse functional roles in the regulation of cellular functions, besides the “classical” role of pituitary function regulation.
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Lajkó, Eszter, Éva Pállinger, Zsombor Kovács, Ildikó Szabó, and László Kőhidai. "Effects of Gonadotropin-Releasing Hormone (GnRH) and Its Analogues on the Physiological Behaviors and Hormone Content of Tetrahymena pyriformis." International Journal of Molecular Sciences 20, no. 22 (November 14, 2019): 5711. http://dx.doi.org/10.3390/ijms20225711.
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The unicellular Tetrahymena distinguishes structure-related vertebrate hormones by its chemosensory reactions. In the present work, the selectivity of hormone receptors was evaluated by analyzing the effects of various gonadotropin-releasing hormone (GnRH) analogs (GnRH-I, GnRH-III) as well as truncated (Ac-SHDWKPG-NH2) and dimer derivatives ([GnRH-III(C)]2 and [GnRH-III(CGFLG)]2) of GnRH-III on (i) locomotory behaviors, (ii) cell proliferation, and (iii) intracellular hormone contents of Tetrahymena pyriformis. The migration, intracellular hormone content, and proliferation of Tetrahymena were investigated by microscope-assisted tracking analysis, flow cytometry, and a CASY TT cell counter, respectively. Depending on the length of linker sequence between the two GnRH-III monomers, the GnRH-III dimers had the opposite effect on Tetrahymena migration. [GnRH-III(CGFLG)]2 dimer had a slow, serpentine-like movement, while [GnRH-III(C)]2 dimer had a rather linear swimming pattern. All GnRH-III derivatives significantly induced cell growth after 6 h incubation. Endogenous histamine content was uniformly enhanced by Ac-SHDWKPG-NH2 and GnRH-III dimers, while some differences between the hormonal activities of GnRHs were manifested in their effects on intracellular levels of serotonin and endorphin. The GnRH peptides could directly affect Tetrahymena migration and proliferation in a structure-dependent manner, and they could indirectly regulate these reactions by paracrine/autocrine mechanisms. Present results support the theory that recognition ability and selectivity of mammalian hormone receptors can be deduced from a phylogenetically ancient level like the unicellular Tetrahymena.
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Tasaka, K., N. Masumoto, J. Mizuki, Y. Ikebuchi, M. Ohmichi, H. Kurachi, A. Miyake, and Y. Murata. "Rab3B is essential for GnRH-induced gonadotrophin release from anterior pituitary cells." Journal of Endocrinology 157, no. 2 (May 1, 1998): 267–74. http://dx.doi.org/10.1677/joe.0.1570267.
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Gonadotrophin-releasing hormone (GnRH) induces the release of gonadotrophins via an increase in cytosolic Ca2+ concentration ([Ca2+]). Rab3B, a member of the small GTP-binding protein Rab family, is known to be involved in Ca(2+)-regulated exocytosis in pituitary cells. However, it is not known whether Rab3B functions in the physiological process regulated by GnRH in gonadotrophs. In this study using antisense oligonucleotide against Rab3B (AS-Rab3B) we determined that Rab3B is involved in GnRH-induced gonadotrophin release. Rab3B immunopositive cells were reduced in 24% of pituitary cells by AS-Rab3B. This treatment did not affect the population of gonadotrophs or the intracellular contents of gonadotrophins. However, AS-Rab3B significantly inhibited the total amount of basal and GnRH-induced gonadotrophin released from pituitary cells. These results show that Rab3B is involved in basal and GnRH-induced gonadotrophins release but not the storage of gonadotrophins. Next, the changes in [Ca2+] and exocytosis in gonadotrophs treated with AS-Rab3B were compared among Rab3B-positive and -negative cells. The change in [Ca2+] was not different in the two groups, but exocytosis was significantly inhibited in Rab3B-negative cells. These results suggest that Rab3B is essential for GnRH-regulated exocytosis downstream of cytosolic Ca2+ in gonadotrophs.
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Edwards, Alun L., M. Sarah Rose, Lois E. Donovan, and Gordon T. Ford. "Premenstrual Exacerbation of Life-Threatening Asthma: Effect of Gonadotrophin Releasing Hormone Analogue Therapy." Canadian Respiratory Journal 3, no. 3 (1996): 203–6. http://dx.doi.org/10.1155/1996/691249.
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Variability in the severity of asthma during various phases of the menstrual cycle has been frequently suspected. However, the hormonal changes that might affect mediators of bronchospasm have yet to be elucidated. The case of a 41-year-old woman suffering from longstanding asthma with life-threatening exacerbations is reported. The patient was treated with buserelin, a gonadotropin releasing hormone (GnRH) analogue, which created a temporary chemical menopause and thus permitted diagnosis of a premenstrual exacerbation of asthma and offered insight into potential therapy. GnRH analogues may therefore be of value in assessing women with severe asthma suspected to vary with the menstrual cycle. The addition of estrogens and progestins at the same time as treatment with GnRH analogue may be of value in determining the role of these hormones in the pathogenesis of menstrually related exacerbations of asthma.
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McArdle, CA, J. Franklin, L. Green, and JN Hislop. "Signalling, cycling and desensitisation of gonadotrophin-releasing hormone receptors." Journal of Endocrinology 173, no. 1 (April 1, 2002): 1–11. http://dx.doi.org/10.1677/joe.0.1730001.
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Sustained stimulation of G-protein-coupled receptors (GPCRs) typically causes receptor desensitisation, which is mediated by phosphorylation, often within the C-terminal tail of the receptor. The consequent binding of beta-arrestin not only prevents the receptor from activating its G protein (causing desensitisation), but can also target it for internalisation via clathrin-coated vesicles and can mediate signalling to proteins regulating endocytosis and mitogen-activated protein kinase (MAPK) cascades. GnRH acts via phospholipase C (PLC)-coupled GPCRs on pituitary gonadotrophs to stimulate a Ca(2+)-mediated increase in gonadotrophin secretion. The type I GnRH receptors (GnRH-Rs), found only in mammals, are unique in that they lack C-terminal tails and apparently do not undergo agonist-induced phosphorylation or bind beta-arrestin; they are therefore resistant to receptor desensitisation and internalise slowly. In contrast, the type II GnRH-Rs, found in numerous vertebrates, possess such tails and show rapid desensitisation and internalisation, with concomitant receptor phosphorylation (within the C-terminal tails) or binding of beta-arrestin, or both. The association with beta-arrestin may also be important for regulation of dynamin, a GTPase that controls separation of endosomes from the plasma membrane. Using recombinant adenovirus to express GnRH-Rs in Hela cells conditionally expressing a dominant negative mutant of dynamin (K44A), we have found that blockade of dynamin-dependent endocytosis inhibits internalisation of type II (xenopus) GnRH-Rs but not type I (human) GnRH-Rs. In these cells, blockade of dynamin-dependent internalisation also inhibited GnRH-R-mediated MAPK activation, but this effect was not receptor specific and therefore not dependent upon dynamin-regulated GnRH-R internalisation. Although type I GnRH-Rs do not desensitise, sustained activation of GnRH-Rs causes desensitisation of gonadotrophin secretion, and we have found that GnRH can cause down-regulation of inositol (1,4,5) trisphosphate receptors and desensitisation of Ca(2+) mobilisation in pituitary cells. The atypical resistance of the GnRH-R to desensitisation may underlie its atypical efficiency at provoking this downstream adaptive response. GnRH-Rs are also expressed in several extrapituitary sites, and these may mediate direct inhibition of proliferation of hormone-dependent cancer cells. Infection with type I GnRH-R-expressing adenovirus facilitated expression of high-affinity, PLC-coupled GnRH-R in mammary and prostate cancer cells, and these mediated pronounced antiproliferative effects of receptor agonists. No such effect was seen in cells transfected with a type II GnRH-R, implying that it is mediated most efficiently by a non-desensitising receptor. Thus it appears that the mammalian GnRH-Rs have undergone a period of rapidly accelerated molecular evolution that is of functional relevance to GnRH-Rs in pituitary and extrapituitary sites.
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Wan, Boyang, Xuejun Yuan, Weiren Yang, Ning Jiao, Yang Li, Faxiao Liu, Mei Liu, Zaibin Yang, Libo Huang, and Shuzhen Jiang. "The Effects of Zearalenone on the Localization and Expression of Reproductive Hormones in the Ovaries of Weaned Gilts." Toxins 13, no. 9 (September 7, 2021): 626. http://dx.doi.org/10.3390/toxins13090626.
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This study aims to investigate the effects of zearalenone (ZEA) on the localizations and expressions of follicle stimulating hormone receptor (FSHR), luteinizing hormone receptor (LHR), gonadotropin releasing hormone (GnRH) and gonadotropin releasing hormone receptor (GnRHR) in the ovaries of weaned gilts. Twenty 42-day-old weaned gilts were randomly allocated into two groups, and treated with a control diet and a ZEA-contaminated diet (ZEA 1.04 mg/kg), respectively. After 7-day adjustment, gilts were fed individually for 35 days and euthanized for blood and ovarian samples collection before morning feeding on the 36th day. Serum hormones of E2, PRG, FSH, LH and GnRH were determined using radioimmunoassay kits. The ovaries were collected for relative mRNA and protein expression, and immunohistochemical analysis of FSHR, LHR, GnRH and GnRHR. The results revealed that ZEA exposure significantly increased the final vulva area (p < 0.05), significantly elevated the serum concentrations of estradiol, follicle stimulating hormone and GnRH (p < 0.05), and markedly up-regulated the mRNA and protein expressions of FSHR, LHR, GnRH and GnRHR (p < 0.05). Besides, the results of immunohistochemistry showed that the immunoreactive substances of ovarian FSHR, LHR, GnRH and GnRHR in the gilts fed the ZEA-contaminated diet were stronger than the gilts fed the control diet. Our findings indicated that dietary ZEA (1.04 mg/kg) could cause follicular proliferation by interfering with the localization and expression of FSHR, LHR, GnRH and GnRHR, and then affect the follicular development of weaned gilts.
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Armansyah, Teuku, Sara Febria Putri, Oppi Oktaviany, Tongku Nizwan Siregar, Syafruddin Syafruddin, Budianto Panjaitan, and Arman Sayuti. "Pemberian Gonadotropin Releasing Hormone Meningkatkan Konsentrasi Hormon Testosteron pada Domba Waringin." Jurnal Veteriner 22, no. 3 (September 30, 2021): 342–51. http://dx.doi.org/10.19087/jveteriner.22.3.342.
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Salah satu upaya untuk meningkatkan konsentrasi testosteron adalah dengan pemberian gonadotropin releasing hormone (GnRH). Peningkatan testosteron menyebabkan peningkatan kualitas spermatozoa. Penelitian ini bertujuan mengetahui pengaruh pemberian gonadotropin releasing hormone (GnRH) terhadap peningkatan kualitas semen dan level testosteron domba waringin. Dalam penelitian ini digunakan tiga ekor domba waringin dengan rancangan pola bujur sangkar latin 3 x 3 sehingga hewan percobaan menerima suntikan NaCl fisiologis sebagai kontrol (K0), 50 ìg GnRH (K1), dan 100 ìg GnRH (K2). Penampungan semen dilakukan satu kali ejakulasi/minggu, selama tiga minggu. Sampel semen dikoleksi menggunakan elektroejakulator 24 jam setelah perlakuan dan diamati warna, konsistensi, volume, motilitas, konsentrasi, viabilitas, dan abnormalitas spermatozoa. Koleksi darah untuk pemeriksaan konsentrasi hormon testosteron dilakukan 60 menit setelah penyuntikan GnRH. Analisis konsentrasi testosteron dilakukan menggunakan metode enzyme linked immunosorbent assay (ELISA). Data mengenai warna dan konsistensi semen dilaporkan secara deskriptif, sedangkan level testosteron, volume semen, motilitas, konsentrasi, viabilitas dan abnormalitas spermatozoa dianalisis dengan analisis varian. Hasil pengamatan menunjukkan bahwa warna dan konsistensi semen yang dikoleksi pada semua kelompok perlakuan adalah krem dengan konsistensi kental. Hasil analisis statistika menunjukkan bahwa volume semen, konsentrasi spermatozoa, motilitas spermatozoa, viabilitas spermatozoa dan abnormalitas spermatozoa setelah pemberian GnRH menunjukkan perbedaan yang tidak signifikan (P>0,05). Rata-rata (±SD) konsentrasi testosteron pada kelompok K0, K1, dan K2 masing-masing adalah 1,82±1,08; 8,05+2,24; dan 8,81±1,09 ng/mL (P<0,05). Disimpulkan bahwa pemberian GnRH tidak memengaruhi kualitas semen namun dapat meningkatkan konsentrasi hormon testosteron pada domba waringin.
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Evans, J. J., and K. J. Catt. "Gonadotrophin-releasing activity of neurohypophysial hormones: II. The pituitary oxytocin receptor mediating gonadotrophin release differs from that of corticotrophs." Journal of Endocrinology 122, no. 1 (July 1989): 107–16. http://dx.doi.org/10.1677/joe.0.1220107.
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ABSTRACT Neurohypophysial hormones stimulate gonadotrophin release from dispersed rat anterior pituitary cells in vitro, acting through receptors distinct from those which mediate the secretory response to gonadotrophin-releasing hormone (GnRH). The LH response to oxytocin was not affected by the presence of the phosphodiesterase inhibitor, methyl isobutylxanthine, but was diminished in the absence of extracellular calcium and was progressively increased as the calcium concentration in the medium was raised to normal. In addition, the calcium channel antagonist, nifedipine, suppressed oxytocin-stimulated secretion of LH. It is likely that the mechanisms of LH release induced by GnRH and neurohypophysial hormones are similar, although stimulation of gonadotrophin secretion is mediated by separate receptor systems. Oxytocin was more active than vasopressin in releasing LH, but less active in releasing ACTH. The highly selective oxytocin agonist, [Thr4,Gly7]oxytocin, elicited concentration-dependent secretion of LH but had little effect on corticotrophin secretion. The neurohypophysial hormone antagonist analogues, [d(CH2)5Tyr(Me)2]-vasopressin, [d(CH2)5Tyr(Me)2,Orn8]vasotocin and [d(CH2)5d-Tyr(Et)2Val4,Cit8]vasopressin, inhibited the LH response to both oxytocin and vasopressin. However, [d(CH2)5Tyr(Me)2]vasopressin was much less effective in inhibiting the ACTH response to the neurohypophysial hormones, and [d(CH2)5Tyr-(Me)2,Orn8]vasotocin and [d(CH2)5d-Tyr(Et)2,Val4, Cit8]vasopressin exhibited no inhibitory activity against ACTH release. Thus, agonist and antagonist analogues of neurophypophysial hormones display divergent activities with regard to LH and ACTH responses, and the neuropeptide receptor mediating gonadotroph activation is clearly different from that on the corticotroph. Whereas the corticotroph receptor is a vasopressin-type receptor an oxytocin-type receptor is responsible for gonadotrophin release by neurohypophysial hormones. Journal of Endocrinology (1989) 122, 107–116
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Gootwine, E., A. Bor, D. Shalhevet, A. Zenou, and R. Braw-Tal. "Differential pituitary response to GnRH in pregnant Booroola-Assaf and Assaf ewes." Reproduction, Fertility and Development 4, no. 2 (1992): 231. http://dx.doi.org/10.1071/rd9920231.
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Pituitary response to exogenous gonadotrophin-releasing hormone (GnRH) was examined at a late stage of pregnancy in 10 Booroola-Assaf ewes heterozygous at the FecB locus (FecBFec+) and in 11 Assaf ewes that were non-carriers (Fec+Fec+). Basal plasma luteinizing hormone (LH) and follicle stimulating hormone (FSH) concentrations were similar in the two genotypes. Administration of 100 micrograms of GnRH resulted in a significant increase (P < 0.05) in plasma LH and FSH concentrations in most of the ewes treated. Maximal responses were observed 105-135 min after GnRH treatment. Pituitary responses to GnRH were significantly lower (P < 0.05) in Booroola-Assaf than in Assaf ewes. The decreased pituitary responsiveness observed in FecB gene carriers compared with Fec+Fec+ ewes might be due to differences in the concentrations of ovarian or uterine hormones modulating the release of gonadotrophin. The results suggest that FecB-specific differences can be observed at the pituitary level.
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McNeilly, J. R., P. Brown, A. J. Clark, and A. S. McNeilly. "Gonadotrophin-releasing hormone modulation of gonadotrophins in the ewe: evidence for differential effects on gene expression and hormone secretion." Journal of Molecular Endocrinology 7, no. 1 (August 1991): 35–43. http://dx.doi.org/10.1677/jme.0.0070035.
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ABSTRACT While the regulation of gonadotrophin secretion by gonadotrophin-releasing hormone (GnRH) has been well documented in both rats and sheep, its role in the synthesis of gonadotrophin subunits remains unclear. We have investigated the effects of the specific inhibition of GnRH by a GnRH agonist on the expression of gonadotrophin subunit genes and the subsequent storage and release of both intact hormones and free α subunit. Treatment with GnRH agonist for 6 weeks abolished pulsatile LH secretion, reduced plasma concentrations of FSH and prevented GnRH-induced release of LH and FSH. This was associated with a reduction of pituitary LH-β mRNA and FSH-β mRNA levels (to 5 and 30% of luteal control values respectively), but not α mRNA which was significantly increased (75% above controls). While there was a small decrease in the pituitary content of FSH (30% of controls), there was a drastic reduction in LH pituitary content (3% of controls). In contrast to the observed rise in α mRNA, there was a decrease in free α subunit in both the pituitary and plasma (to 30 and 80% of control levels). These results suggest that, while GnRH positively regulates the expression of both gonadotrophin β-subunit genes, it can, under certain circumstances, negatively regulate α-subunit gene expression. Despite the complete absence of LH and FSH in response to GnRH, there remained a basal level of β-subunit gene expression and only a modest reduction (50%) in the plasma levels of both FSH and LH, suggesting that there is a basal secretory pathway. The dramatic reduction in LH pituitary content indicates that GnRH is required for the operation of a regulatory/storage pathway for the secretion of LH. There appears to be no similar mechanism for FSH. The LH-specific pathway is probably dependent upon the availability of LH-β subunits which subsequently plays a role in regulating α subunit by sequestering, assembling and storing the intact hormone in the presence of GnRH. Finally, in the absence of responsiveness to GnRH, the regulation of α-subunit production is not at the level of gene transcription. Inefficient translation of the mRNA or rapid degradation of the free α chain may account for the observed dramatic decrease in production of α subunit.
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Junaidi, A., P. E. Williamson, G. B. Martin, P. G. Stanton, M. A. Blackberry, J. M. Cummins, and T. E. Trigg. "Pituitary and testicular endocrine responses to exogenous gonadotrophin-releasing hormone (GnRH) and luteinising hormone in male dogs treated with GnRH agonist implants." Reproduction, Fertility and Development 19, no. 8 (2007): 891. http://dx.doi.org/10.1071/rd07088.
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The present study tested whether exogenous gonadotrophin-releasing hormone (GnRH) and luteinising hormone (LH) can stimulate LH and testosterone secretion in dogs chronically treated with a GnRH superagonist. Twenty male adult dogs were assigned to a completely randomised design comprising five groups of four animals. Each dog in the control group received a blank implant (placebo) and each dog in the other four groups received a 6-mg implant containing a slow-release formulation of deslorelin (d-Trp6-Pro9-des-Gly10–LH-releasing hormone ethylamide). The same four control dogs were used for all hormonal challenges, whereas a different deslorelin-implanted group was used for each challenge. Native GnRH (5 μg kg–1 bodyweight, i.v.) was injected on Days 15, 25, 40 and 100 after implantation, whereas bovine LH (0.5 μg kg–1 bodyweight, i.v.) was injected on Days 16, 26, 41 and 101. On all occasions after Day 25–26 postimplantation, exogenous GnRH and LH elicited higher plasma concentrations of LH and testosterone in control than deslorelin-treated animals (P < 0.05). It was concluded that, in male dogs, implantation of a GnRH superagonist desensitised the pituitary gonadotrophs to GnRH and also led to a desensitisation of the Leydig cells to LH. This explains, at least in part, the profound reduction in the production of androgen and spermatozoa in deslorelin-treated male dogs.
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TRUDEAU, V., A. PHARAZYN, F. X. AHERNE, and E. BELTRANENA. "NALOXONE ELEVATES PLASMA FOLLICLE STIMULATING HORMONE BUT NOT LUTEINIZING HORMONE LEVELS IN THE IMMATURE MALE PIG." Canadian Journal of Animal Science 69, no. 4 (December 1, 1989): 1095–98. http://dx.doi.org/10.4141/cjas89-126.
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The effects of intraperitoneal injection of gonadotropin-releasing hormone (GnRH) alone, naloxone (NAL) alone, or in combination on plasma levels of follicle stimulating hormone (FSH) and luteinizing hormone (LH) was studied in 4- to 5-wk-old male pigs. GnRH (1 μg kg−1) effectively stimulated (P < 0.05) secretion of both gonadotropins whereas NAL (1 and 10 mg kg−1) stimulated only FSH secretion (P < 0.05). There was no interaction between GnRH and NAL on gonadotropin release. These results suggest that endogenous opiates are involved in the regulation of FSH secretion but not LH secretion in the immature male pig. Key words: Follicle-stimulating hormone, luteinizing hormone, naloxone, gonadotropin-releasing hormone, male pig
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McIntosh, J. E. A., and R. P. McIntosh. "Varying the patterns and concentrations of gonadotrophin-releasing hormone stimulation does not alter the ratio of LH and FSH released from perifused sheep pituitary cells." Journal of Endocrinology 109, no. 2 (May 1986): 155–61. http://dx.doi.org/10.1677/joe.0.1090155.
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ABSTRACT Our aim was to determine whether release of LH and FSH can be controlled differentially by the characteristics of applied signals of stimulatory gonadotrophin-releasing hormone (GnRH) alone, free of the effects of steroid feedback or other influences from the whole animal. The outputs of both gonadotrophins were significantly correlated (r≈0·90; P<0·0005) when samples of freshly dispersed sheep pituitary cells were perifused in columns for 7 h with medium containing a range of concentrations of GnRH in various patterns of pulses. Hormone released in response to the second, third and fourth pulses from every column was analysed in detail. Dose–response relationships for both LH and FSH were very similar when cells were stimulated with 5–8500 pmol GnRH/1 in 5-min pulses every hour. When GnRH was delivered in pulses at a maximally stimulating level, the outputs of both hormones increased similarly with increasing inter-pulse intervals. Efficiency of stimulation (release of gonadotrophin/unit stimulatory GnRH) decreased (was desensitized) with increasing pulse duration in the same way for both hormones. Thus, varying the dose, interval and duration of GnRH pulses did not alter the proportions of LH and FSH released in the short-term from freshly dissociated cells. However, the same cell preparations released more LH relative to FSH when treated with maximally stimulating levels of GnRH for 3 h in the presence of 10% serum from a sheep in the follicular phase of its ovulatory cycle compared with charcoal-treated serum. Because there was no gonadotrophin synthesis under the conditions used in vitro these results suggest that changes in the LH/FSH ratio seen in whole animals are more likely to result from differential clearance from the circulation, ovarian feedback at the pituitary, differential synthesis in intact tissue or another hormone influencing FSH secretion, rather than from differences in the mechanism of acute release controlled by GnRH. J. Endocr. (1986) 109, 155–161
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Tena-Sempere, Manuel, and Ilpo Huhtaniemi. "Sex in the brain: How the brain regulates reproductive function." Biochemist 31, no. 2 (April 1, 2009): 4–7. http://dx.doi.org/10.1042/bio03102004.
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Reproductive functions are maintained by a complex hormonal regulatory network called the hypothalamic–pituitary–gonadal (HPG) axis, which is under the hierarchical control of a network of neurohormones that ultimately modulate the synthesis and pulsatile release of the decapeptide gonadotropin-releasing hormone (GnRH) by specialized neural cells distributed along the mediobasal hypothalamus. This neuropeptide drives the production of the two gonadotropic hormones of the anterior pituitary gland, luteinizing hormone (LH) and folliclestimulating hormone (FSH), which are released into the circulation and regulate specific functions of the ovary and testis. In turn, hormones produced by the gonads feed back to the hypothalamic– pituitary level to maintain functional balance of the HPG axis, through negative and positive (only in females) regulatory loops. In this article, we review the main hormonal regulatory systems that are operative in the HPG axis with special emphasis on recent developments in our knowledge of the neuroendocrine pathways governing GnRH secretion, including the identification of kisspeptins and G-protein-coupled receptor 54 (GPR54) as major gatekeepers of puberty onset and fertility.
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Romerowicz-Misielak, Maria, and Marek Koziorowski. "The Gonadotropins Subunits, GNRH and GNRH Receptor Gene Expression and Role of Carbon Monoxide in Seasonal Breeding Animals." Annals of Animal Science 12, no. 1 (November 1, 2012): 15–23. http://dx.doi.org/10.2478/v10220-012-0002-x.
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The Gonadotropins Subunits, GNRH and GNRH Receptor Gene Expression and Role of Carbon Monoxide in Seasonal Breeding AnimalsSeasonality in reproduction occurs mainly in wild species and it is the result of natural selection. Signals to start or finish the period of reproductive activity, both environmental and hormonal depend on the neuroendocrine pathway - synthesis and secretion of pituitary hormones, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), under the control of the hypothalamic gonadotropin-releasing hormone (GnRH) neurons. Variable frequency of GnRH pulses is not only the main factor governing primary and preovulatory release of gonadotropins, but it can also play a role in the specific transcriptional activity of gonadotropin subunit genes (LHβ, FSHβ and Cga). However, changes in release of GnRH pulse pattern do not explain the preferential stimulation of the synthesis and secretion of gonadotropins in the annual reproductive cycle. In this regulation also a GnRH independent mechanism participates. It seems that the main factor responsible for the occurrence of the seasonal modulation of reproduction in sheep and other mammals, is significant changes in response of GnRH systems to gonadal steroids. The effect of carbon monoxide on regulation of the hypothalamic-pituitary-gonadal axis has not been studied to date. There is substantial evidence to suggest that it may play a role in the transduction of information on day length. The presence of heme oxygenase-2 in hypothalamic areas important for regulation of pituitary secretory function and in the pituitary itself suggests that carbon monoxide, the product of this enzyme, may participate in the regulation of hormone secretion by the pineal gland.
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Braden, Tim D., and P. Michael Conn. "The 1990 James A. F. Stevenson Memorial Lecture. Gonadotropin-releasing hormone and its actions." Canadian Journal of Physiology and Pharmacology 69, no. 4 (April 1, 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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Clarke, I. J., and J. T. Cummins. "The significance of small pulses of gonadotrophin-releasing hormone." Journal of Endocrinology 113, no. 3 (June 1987): 413–18. http://dx.doi.org/10.1677/joe.0.1130413.
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ABSTRACT A series of experiments was conducted to ascertain the significance of 'small' pulses of gonadotrophin-releasing hormone (GnRH). In the first experiment, ovariectomized hypothalamo-pituitary disconnected (HPD) ewes were given 250 ng pulses of GnRH every 2 h for 1 week, 25 ng pulses every 2 h for 24 h, 25 ng pulses hourly for 24 h and then alternating hourly pulses of 25 and 250 ng. During the 25 ng pulses, LH was not detectable in plasma and FSH concentrations declined after 2 days. Following the 25 ng pulses, the resumption of 250 ng pulses led to exaggerated LH responses (mean ± s.e.m. pulse amplitude 18·7 ± 1·7 vs 10·2 ± 1·2 μg/l in the first week). In a second experiment, ovariectomized–HPD ewes were maintained on 250 ng GnRH pulses every 2 h for 1 week and were then given three 25 ng pulses mid-way between the 250 ng pulses. Samples of blood were taken over three 250 ng pulses without 25 ng insertions and over three pulses with insertions. The insertion of 25 ng GnRH pulses did not cause LH pulses in their own right and did not alter the LH responses to the 250 ng pulses. In a third experiment, 50 ng GnRH pulses were inserted between the 250 ng GnRH pulses, as in experiment 2; these 50 ng pulses caused small LH pulses and led to a reduction in the response of the LH pulse amplitude to the 250 ng pulses. The 'small' LH pulses which occurred in response to 50 ng GnRH compensated for the reduced responses to the 250 ng pulses. Hence, the integrated area under the LH curve and between successive 250 ng pulses remained the same, irrespective of the 50 ng insertions. From these data we conclude that 'small' GnRH pulses alone can sustain ongoing LH synthesis without release, leading to an accumulation of releasable LH, and that the insertion of 'small' GnRH pulses may modify the pattern of pituitary responsiveness to 'large' GnRH pulses. J. Endocr. (1987) 113, 413–418
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Ohlsson, Bodil. "Gonadotropin-Releasing Hormone and Its Physiological and Pathophysiological Roles in Relation to the Structure and Function of the Gastrointestinal Tract." European Surgical Research 57, no. 1-2 (2016): 22–33. http://dx.doi.org/10.1159/000445717.
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Background: Gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH), and luteinizing hormone (LH) are involved in the reproductive cycle and regulate the secretion of sex steroids from the gonads. In mammals, GnRH1 is secreted as a hormone from the hypothalamus, whereas both GnRH1 and GnRH2 are present as neuropeptides in a variety of tissues. This review describes the role of GnRH in the gastrointestinal tract. Summary: GnRH1, GnRH2, and LH receptors in humans and rats, and GnRH receptors in rats, have been described in the gastrointestinal tract, where they affect motility, gastric and hormone secretion, and cell proliferation. GnRH analogs are clinically used in the treatment of sex hormone-dependent diseases, i.e., endometriosis and malignancies, and as pretreatments for in vitro fertilization. Severe gastrointestinal dysmotility has been shown to develop in some women after such treatment, along with a reduction in the number of enteric neurons and autoantibodies against GnRH. Consequently, a rat model of enteric neurodegeneration has been developed based on the administration of the GnRH analog buserelin. Serum IgM antibodies against GnRH1, the GnRH2 precursor progonadoliberin-2, and the GnRH receptor have also been described in patients with irritable bowel syndrome and dysmotility, as well as in patients with gastrointestinal disorders associated with diabetes mellitus, posterior laryngitis, and primary Sjögren's syndrome, although no treatments using GnRH analogs have been administered. Conclusion: GnRH and receptors for GnRH and LH are present in the human and rat gastrointestinal tract. Treatment with GnRH analogs may induce severe dysmotility, and a rat model of enteric neurodegeneration has been developed based on stimulation by the GnRH analog buserelin. Autoantibodies against GnRH and its receptor are found in a subgroup of patients with functional bowel disorders and dysmotility, independent of treatment with GnRH analogs.
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Harrison, G. S., M. E. Wierman, T. M. Nett, and L. M. Glode. "Gonadotropin-releasing hormone and its receptor in normal and malignant cells." Endocrine-Related Cancer 11, no. 4 (December 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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Sahadan, Fatin Nabilah, Annie Christianus, Ina-Salwany Md Yasin, Fadhil-Syukri Ismail, Roshani Othman, and Zarirah Zulperi. "Gonadotropin-Releasing Hormone (GnRH)- Its Approaches to Improve Reproduction in Fish." Sains Malaysiana 51, no. 11 (November 30, 2021): 3539–49. http://dx.doi.org/10.17576/jsm-2022-5111-03.
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This review briefly highlights previous studies on the gonadotropin-releasing hormone (GnRH) and its approaches to improving fish reproduction in the aquaculture industry. Reproductive system dysfunction of the captive fish is the main problem that has to be treated depending on the compatibility of fish species. This problem is caused by the non-synchronized maturation of female and male broodstock, and the low quality of broodstock. As shown in previous studies, induced breeding with exogenous treatment from specialized hormones could be one of the best cures for this issue. Hormonal treatments have been used by farmers to overcome the reproductive system dysfunctions in establishing captive wild or hatchery-based breeding. Although the imitation in its natural condition has been set up, for broodstock to spawn naturally problems still occur, hence the need for hormonal therapy. This review aims to deliver the results and contributions of an established artificial hormone, gonadotropin-releasing hormone analogue (GnRHa), to treat fish reproductive system dysfunction, to improve the qualities of eggs, seedlings, and broodstock, mainly to help fish farmers and can be used in the aquaculture industry to improve the reproduction of cultured fishes for sustainable aquaculture production to achieve the market demand and consumption.
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Weng, Shun-Long, Shu-Ling Tzeng, Chun-I. Lee, Chung-Hsien Liu, Chun-Chia Huang, Shun-Fa Yang, Maw-Sheng Lee, and Tsung-Hsien Lee. "Association between GnRH Receptor Polymorphisms and Luteinizing Hormone Levels for Low Ovarian Reserve Infertile Women." International Journal of Environmental Research and Public Health 18, no. 13 (June 30, 2021): 7006. http://dx.doi.org/10.3390/ijerph18137006.
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The choice of ovarian stimulation protocols in assisted reproduction technology (ART) cycles for low ovarian reserve patients is challenging. Our previous report indicated that the gonadotrophin-releasing (GnRH) agonist (GnRHa) protocol is better than the GnRH antagonist (GnRHant) protocol for young age poor responders. Here, we recruited 269 patients with anti-Müllerian hormone (AMH) < 1.2 ng/mL undergoing their first ART cycles for this nested case-control study. We investigated the genetic variants of the relevant genes, including follicular stimulating hormone receptor (FSHR; rs6166), AMH (rs10407022), GnRH (rs6185), and GnRH receptor (GnRHR; rs3756159) in patients <35 years (n = 86) and patients ≥35 years of age (n = 183). Only the genotype of GnRHR (rs3756159) is distributed differently in young (CC 39.5%, CT/TT 60.5%) versus advanced (CC 24.0%, CT/TT 76.0%) age groups (recessive model, p = 0.0091). Furthermore, the baseline luteinizing hormone (LH) levels (3.60 (2.45 to 5.40) vs. 4.40 (2.91 to 6.48)) are different between CC and CT/TT genotype of GnRHR (rs3756159). In conclusion, the genetic variants of GnRHR (rs3756159) could modulate the release of LH in the pituitary gland and might then affect the outcome of ovarian stimulation by GnRHant or GnRHa protocols for patients with low AMH levels.
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Chesnokova, Vera, and Shlomo Melmed. "Peptide Hormone Regulation of DNA Damage Responses." Endocrine Reviews 41, no. 4 (April 9, 2020): 519–37. http://dx.doi.org/10.1210/endrev/bnaa009.
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Abstract DNA damage response (DDR) and DNA repair pathways determine neoplastic cell transformation and therapeutic responses, as well as the aging process. Altered DDR functioning results in accumulation of unrepaired DNA damage, increased frequency of tumorigenic mutations, and premature aging. Recent evidence suggests that polypeptide hormones play a role in modulating DDR and DNA damage repair, while DNA damage accumulation may also affect hormonal status. We review the available reports elucidating involvement of insulin-like growth factor 1 (IGF1), growth hormone (GH), α-melanocyte stimulating hormone (αMSH), and gonadotropin-releasing hormone (GnRH)/gonadotropins in DDR and DNA repair as well as the current understanding of pathways enabling these actions. We discuss effects of DNA damage pathway mutations, including Fanconi anemia, on endocrine function and consider mechanisms underlying these phenotypes. (Endocrine Reviews 41: 1 – 19, 2020)
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Ferasyi, T. R., H. Barrett, D. Blache, and G. B. Martin. "279. A dynamic model of the control of pulsatile luteinizing hormone secretion by gonadotrophin-releasing hormone." Reproduction, Fertility and Development 17, no. 9 (2005): 116. http://dx.doi.org/10.1071/srb05abs279.
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Infusion of GnRH in a continuous manner or with a very high pulse frequency initially stimulates but then downregulates LH secretion.1,2 This phenomenon is caused by the slow rate of internalisation of the GnRH receptor (GnRH-R) and the subsequent slow return of receptors to the plasma membrane of the gonadotroph.3 Pulsatile release of GnRH overcomes this problem by allowing a delay between successive stimulations. It is difficult to determine the relative importance of critical control points in this process in an animal model because GnRH activity reflects integrated inputs from many internal and external factors. We are therefore using SAAM II software to develop a compartmental model of the relationship between GnRH-R availability and LH responses following changes in GnRH pulse frequency. The model has three receptor states (free, bound, and internalised) and one LH compartment (Fig. 1). We assumed LH release is a function of the amount of receptor that binds GnRH. Following GnRH binding, receptors are rapidly lost as they enter the internalised state and then slowly returned to the membrane surface. We further assumed that the slow rate of receptor return explains the decrease in LH response with very high frequencies of GnRH pulses. The values for parameters were based on data obtained from experiments with sheep. In our current version of the model, downregulation is observed when gonadotrophs are stimulated with GnRH pulses every 15 min (Fig. 1), but not with pulses every 30 or 60 min, at a slow recycling rate (0.004 min–1). In contrast, LH secretion increases when GnRH is pulsed every 15 min and recycling rate is increased to 0.04 min–1. This suggests that, in sheep, a recycling rate between 0.004 and 0.04 min–1 is a critical aspect of the intracellular control of the process. Future work will include steroid feedback loops.
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Ubuka, Takayoshi, Stephanie Kim, Yu-chi Huang, Jessica Reid, Jennifer Jiang, Tomohiro Osugi, Vishwajit S. Chowdhury, Kazuyoshi Tsutsui, and George E. Bentley. "Gonadotropin-Inhibitory Hormone Neurons Interact Directly with Gonadotropin-Releasing Hormone-I and -II Neurons in European Starling Brain." Endocrinology 149, no. 1 (September 27, 2007): 268–78. http://dx.doi.org/10.1210/en.2007-0983.
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Gonadotropin-inhibitory hormone (GnIH) is a hypothalamic dodecapeptide (SIKPSAYLPLRF-NH2) that directly inhibits gonadotropin synthesis and release from quail pituitary. The action of GnIH is mediated by a novel G-protein coupled receptor. This gonadotropin-inhibitory system may be widespread in vertebrates, at least birds and mammals. In these higher vertebrates, histological evidence suggests contact of GnIH immunoreactive axon terminals with GnRH neurons, thus indicating direct regulation of GnRH neuronal activity by GnIH. In this study we investigated the interaction of GnIH and GnRH-I and -II neurons in European starling (Sturnus vulgaris) brain. Cloned starling GnIH precursor cDNA encoded three peptides that possess characteristic LPXRF-amide (X = L or Q) motifs at the C termini. Starling GnIH was further identified as SIKPFANLPLRF-NH2 by mass spectrometry combined with immunoaffinity purification. GnIH neurons, identified by in situ hybridization and immunocytochemistry (ICC), were clustered in the hypothalamic paraventricular nucleus. GnIH immunoreactive fiber terminals were present in the external layer of the median eminence in addition to the preoptic area and midbrain, where GnRH-I and GnRH-II neuronal cell bodies exist, respectively. GnIH axon terminals on GnRH-I and -II neurons were shown by GnIH and GnRH double-label ICC. Furthermore, the expression of starling GnIH receptor mRNA was identified in both GnRH-I and GnRH-II neurons by in situ hybridization combined with GnRH ICC. The cellular localization of GnIH receptor has not previously been identified in any vertebrate brain. Thus, GnIH may regulate reproduction of vertebrates by directly modulating GnRH-I and GnRH-II neuronal activity, in addition to influencing the pituitary gland.
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Ortmann, O., JM Weiss, and K. Diedrich. "Gonadotrophin-releasing hormone (GnRH) and GnRH agonists: mechanisms of action." Reproductive BioMedicine Online 5 (January 2002): 1–7. http://dx.doi.org/10.1016/s1472-6483(11)60210-1.
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Birnie, L. M., P. J. Broadbent, J. S. M. Hutchinson, R. G. Watt, and D. F. Dolman. "Effects of gonadotrophin releasing hormone agonist treatment on oestrous cycle length and superovulatory response in maiden heifers." Proceedings of the British Society of Animal Science 1995 (March 1995): 141. http://dx.doi.org/10.1017/s1752756200591364.
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Current variability in superovulatory response prevents the economical production of large numbers of high quality embryos and limits the use of embryo transfer. Pulsatile administration of GnRH (gonadotrophin releasing hormone) elicits pulsatile secretion of LH (luteinising hormone) while chronic treatment with a potent GnRH agonist reduces LH secretion. Using the latter, gonadotrophin-dependent preovulatory antral follicle development may be suppressed, resulting in a uniform cohort of small antral follicles in the absence of a dominant follicle which could then be superstimulated by exogenous gonadotrophin.
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Birnie, L. M., P. J. Broadbent, J. S. M. Hutchinson, R. G. Watt, and D. F. Dolman. "Effects of gonadotrophin releasing hormone agonist treatment on oestrous cycle length and superovulatory response in maiden heifers." Proceedings of the British Society of Animal Science 1995 (March 1995): 141. http://dx.doi.org/10.1017/s030822960002907x.
Full textAbstract:
Current variability in superovulatory response prevents the economical production of large numbers of high quality embryos and limits the use of embryo transfer. Pulsatile administration of GnRH (gonadotrophin releasing hormone) elicits pulsatile secretion of LH (luteinising hormone) while chronic treatment with a potent GnRH agonist reduces LH secretion. Using the latter, gonadotrophin-dependent preovulatory antral follicle development may be suppressed, resulting in a uniform cohort of small antral follicles in the absence of a dominant follicle which could then be superstimulated by exogenous gonadotrophin.
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Scaletscky, Renato, and Joseph A. Smith. "Disease Flare with Gonadotrophin-Releasing Hormone (GnRH) Analogues." Drug Safety 8, no. 4 (April 1993): 265–70. http://dx.doi.org/10.2165/00002018-199308040-00001.
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Anderson, L., G. Milligan, and K. A. Eidne. "Characterization of the gonadotrophin-releasing hormone receptor in αT3-1 pituitary gonadotroph cells." Journal of Endocrinology 136, no. 1 (January 1993): 51—NP. http://dx.doi.org/10.1677/joe.0.1360051.
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ABSTRACT The present study has characterized the gonadotrophin-releasing hormone (GnRH) receptor in immortalized αT3-1 pituitary gonadotroph cells. GnRH and GnRH analogues produced both a dose- and time-dependent increase in total inositol phosphate (IP) accumulation. The rank order of potency of these analogues was the same as that obtained in parallel receptor-binding studies in αT3-1 cells. These responses were abolished following pretreatment with a GnRH antagonist. The use of a specific inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) assay demonstrated a rapid but short-lived rise in Ins(1,4,5)P3 production. Intracellular calcium ([Ca2+]i) was subsequently measured in αT3-1 cells using dual wavelength fluorescence microscopy combined with dynamic video imaging. GnRH produced a biphasic rise in [Ca2+]i. The initial calcium transient was complete within seconds while the smaller secondary plateau phase lasted several minutes. G-protein involvement in the IP response to GnRH in αT3-1 cells was investigated using sodium fluoride (NaF) and pertussis toxin (PTx) which activate and inactivate G-proteins respectively. Like GnRH, NaF produced a dose- and time-dependent increase in IP accumulation. Activation of phospholipase C in these cells by either GnRH or NaF was PTx-insensitive, suggesting that the G-protein involved was neither Gi nor Go but more probably Gq. Immunoblot analysis of αT3-1 cell membranes using antisera raised against the predicted C-terminal decapeptide of the α subunit of Gq demonstrated the presence of Gq in αT3-1 cells. Collectively these results show that the GnRH receptors expressed in αT3-1 cells are coupled to the phosphatidylinositol second messenger pathway via a specific G-protein. αT3-1 therefore represents a convenient model in which to study GnRH-related second messenger pathways. Journal of Endocrinology (1993) 136, 51–58
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Pinilla, L., P. Garnelo, M. Tena-Sempere, F. Gaytan, and E. Aguilar. "Mechanisms of reproductive deficiency in male rats treated neonatally with a gonadotrophin-releasing hormone antagonist." Journal of Endocrinology 142, no. 3 (September 1994): 517–25. http://dx.doi.org/10.1677/joe.0.1420517.
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Abstract It is well known that males injected neonatally with oestradiol or antiserum or antagonists (ANT) against gonadotrophin-releasing hormone (GnRH) show multiple reproductive disorders. In the present work, in males treated neonatally with GnRH-ANT, we have analysed: (1) whether the impairment of reproductive function can be blocked by simultaneous treatment with gonadotrophins, (2) the possible differences in the effects of GnRH-ANT injected before or after the proliferation of Sertoli cells which takes place between days 1 and 15 of age, and (3) the mechanism(s) for the increased FSH secretion observed in adulthood. Experimental designs included: administration of GnRH-ANT between days 1 and 16 or 15 and 30 of age, simultaneous administration of gonadotrophins and GnRH-ANT to neonatal males, and measurement of FSH secretion after orchidectomy or specific destruction of Leydig cells with ethylene dimethane sulphonate (EDS) in adult males treated neonatally with GnRH-ANT. The principal new data presented in our studies are the following: (1) delayed puberty was observed not only in males injected neonatally with GnRH-ANT, but also in those injected with gonadotrophins or with GnRH-ANT and gonadotrophins, (2) the decreased fertility and increased FSH secretion observed in adult males treated neonatally with GnRH-ANT were normalized by simultaneous administration of GnRH-ANT and gonadotrophins, and (3) the increased FSH secretion in adult males treated neonatally with GnRH-ANT remained after EDS or orchidectomy, suggesting that mechanisms other than decreased inhibin secretion were involved in the increased secretion of FSH. Journal of Endocrinology (1994) 142, 517–525
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Naik, S. I., G. Saade, A. Detta, and R. N. Clayton. "Homologous ligand regulation of gonadotrophin-releasing hormone receptors in vivo: relationship to gonadotrophin secretion and gonadal steroids." Journal of Endocrinology 107, no. 1 (October 1985): 41–47. http://dx.doi.org/10.1677/joe.0.1070041.
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ABSTRACT A single injection of gonadotrophin-releasing hormone (GnRH) (60 ng s.c., 42·9 nmol) induced biphasic GnRH receptor regulation in normal intact adult female mice. A transient 22% receptor decrease occurred 30–60 min after injection of GnRH when peak serum decapeptide concentrations were reached (137 ± 41 (s.e.m.) ng/l). This GnRH receptor decrease occurred shortly after the peak serum LH values at 15–30 min. The subsequent rapid (within 1 h) return of GnRH receptor levels to normal suggested transient receptor occupancy by GnRH rather than true receptor loss. At 8 h after injection of GnRH a significant 35% increase in GnRH receptors was consistently observed, when serum GnRH levels were undetectable and serum LH had returned to basal levels. This receptor increase was not due to increased receptor affinity, and was prevented by a non-specific protein synthesis inhibitor. Ovariectomy, which caused a 50% fall in GnRH receptors (59·4 ± 4·9 fmol/pituitary gland in intact controls; 26·9 ± 2·6 in ovariectomized mice) abolished the induction by GnRH of its own receptors, although the initial transient decrease occurred over the period of the acute serum LH and FSH rise. Despite a 50% reduction in GnRH receptors in ovariectomized mice, increased serum gonadotrophin levels and responsiveness to GnRH were maintained, indicating dissociation between receptor changes and gonadotrophin levels. No GnRH receptor up-regulation was observed 8 h after a single GnRH injection (60 ng s.c.) in either intact or orchidectomized normal male mice. However, the same treatment doubled GnRH receptors in GnRH-deficient (hpg) female mice. While GnRH appears to up-regulate its own receptors by a direct action on pituitary gonadotrophs in the GnRH-deficient mouse its action in the normal female mouse pituitary appears secondary to stimulation of a gonadal product, presumably oestrogens. J. Endocr. (1985) 107, 41–47
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Tzoupis, Haralambos, Agathi Nteli, Maria-Eleni Androutsou, and Theodore Tselios. "Gonadotropin-Releasing Hormone and GnRH Receptor: Structure, Function and Drug Development." Current Medicinal Chemistry 27, no. 36 (November 4, 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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Kanda, Shinji, Kei Nishikawa, Tomomi Karigo, Kataaki Okubo, Shoko Isomae, Hideki Abe, Daisuke Kobayashi, and Yoshitaka Oka. "Regular Pacemaker Activity Characterizes Gonadotropin-Releasing Hormone 2 Neurons Recorded from Green Fluorescent Protein-Transgenic Medaka." Endocrinology 151, no. 2 (February 1, 2010): 695–701. http://dx.doi.org/10.1210/en.2009-0842.
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GnRH2 is a molecule conserved from fish to humans, suggesting its important functions. However, recent studies have shown that GnRH2 neurons project widely in the brain but not to the pituitary, which suggests their functions other than stimulation of gonadotropin secretion. In contrast to the wealth of knowledge in GnRH1 and GnRH3 neuronal systems, the GnRH2 neuronal system remains to be studied, and there has been no single cell approach so far, partly because of the lack of GnRH2 system in rodents. Here, we generated GnRH2-green fluorescent protein (GFP) transgenic medaka for the first single cell electrophysiological recording from GnRH2 neurons in vertebrates. Whole-cell and on-cell patch clamp analyses revealed their regular pacemaker activities that are intrinsic to the GnRH2 neurons. Pacemaker activities of GnRH2 neurons were not peculiar to medaka because dwarf gourami GnRH2 neurons also showed similar pacemaker activities. By comparing with spontaneous action currents from GFP-expressing GnRH1 and GnRH3 neurons in the adult transgenic medaka, which were already in our hands, we have demonstrated that GnRH2 neurons show pacemaker activity similar to nonhypophysiotropic GnRH3 neurons but not to hypophysiotropic GnRH1 neurons. Thus, by taking advantage of medaka brain, which has all three GnRH neuronal systems with different axonal projection patterns and thus different functions, we have gained insights into the close relationship between the pattern of spontaneous electrical activity and the functions of the three. Moreover, the three types of GnRH-GFP transgenic medaka will provide useful models for studying multifunctional GnRH systems in future.
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Kereilwe, Onalenna, Kiran Pandey, Vitaliano Borromeo, and Hiroya Kadokawa. "Anti-Müllerian hormone receptor type 2 is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion." Reproduction, Fertility and Development 30, no. 9 (2018): 1192. http://dx.doi.org/10.1071/rd17377.
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Preantral and small antral follicles may secret anti-Müllerian hormone (AMH) to control gonadotrophin secretion from ruminant gonadotrophs. The present study investigated whether the main receptor for AMH, AMH receptor type 2 (AMHR2), is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion. Expression of AMHR2 mRNA was detected in anterior pituitaries (APs) of postpubertal heifers using reverse transcription–polymerase chain reaction. An anti-AMHR2 chicken antibody was developed against the extracellular region near the N-terminus of bovine AMHR2. Western blotting using this antibody detected the expression of AMHR2 protein in APs. Immunofluorescence microscopy using the same antibody visualised colocalisation of AMHR2 with gonadotrophin-releasing hormone (GnRH) receptor on the plasma membrane of gonadotrophs. AP cells were cultured for 3.5 days and then treated with increasing concentrations (0, 1, 10, 100, or 1000 pg mL−1) of AMH. AMH (10–1000 pg mL−1) stimulated (P < 0.05) basal FSH secretion. In addition, AMH (100–1000 pg mL−1) weakly stimulated (P < 0.05) basal LH secretion. AMH (100–1000 pg mL−1) inhibited GnRH-induced FSH secretion, but not GnRH-induced LH secretion, in AP cells. In conclusion, AMHR2 is expressed in gonadotrophs of postpubertal heifers to control gonadotrophin secretion.
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Ciechanowska, Magdalena, Magdalena Łapot, Tadeusz Malewski, Krystyna Mateusiak, Tomasz Misztal, and Franciszek Przekop. "Effects of corticotropin-releasing hormone and its antagonist on the gene expression of gonadotrophin-releasing hormone (GnRH) and GnRH receptor in the hypothalamus and anterior pituitary gland of follicular phase ewes." Reproduction, Fertility and Development 23, no. 6 (2011): 780. http://dx.doi.org/10.1071/rd10341.
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There is no information in the literature regarding the effect of corticotropin-releasing hormone (CRH) on genes encoding gonadotrophin-releasing hormone (GnRH) and the GnRH receptor (GnRHR) in the hypothalamus or on GnRHR gene expression in the pituitary gland in vivo. Thus, the aim of the present study was to investigate, in follicular phase ewes, the effects of prolonged, intermittent infusion of small doses of CRH or its antagonist (α-helical CRH 9-41; CRH-A) into the third cerebral ventricle on GnRH mRNA and GnRHR mRNA levels in the hypothalamo–pituitary unit and on LH secretion. Stimulation or inhibition of CRH receptors significantly decreased or increased GnRH gene expression in the hypothalamus, respectively, and led to different responses in GnRHR gene expression in discrete hypothalamic areas. For example, CRH increased GnRHR gene expression in the preoptic area, but decreased it in the hypothalamus/stalk median eminence and in the anterior pituitary gland. In addition, CRH decreased LH secretion. Blockade of CRH receptors had the opposite effect on GnRHR gene expression. The results suggest that activation of CRH receptors in the hypothalamus of follicular phase ewes can modulate the biosynthesis and release of GnRH through complex changes in the expression of GnRH and GnRHR genes in the hypothalamo–anterior pituitary unit.
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Graham, KE, KD Nusser, and MJ Low. "LbetaT2 gonadotroph cells secrete follicle stimulating hormone (FSH) in response to active A." Journal of Endocrinology 162, no. 3 (September 1, 1999): R1—R5. http://dx.doi.org/10.1677/joe.0.162r001.
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Secretion of luteinizing hormone in response to gonadotropin releasing hormone (GnRH) has been described in the recently developed LbetaT2 gonadotroph cell line. We evaluated the expression of follicle stimulating hormone (FSH)beta mRNA and secretion of FSH from LbetaT2 cells in response to GnRH and activin A. LbetaT2 cells were treated with activin A in doses from 0 to 50 ng/ml, with or without a daily 10 nM GnRH pulse, or with GnRH alone. FSH secretion was stimulated over 6-fold by concomitant GnRH and activin A in a dose-responsive fashion at 72 h of treatment. FSHbeta mRNA was detectable by ribonuclease protection assay only in cells treated with activin A with or without GnRH. The demonstration of FSHbeta gene expression in LbetaT2 cells further validates these cells as mature, differentiated gonadotrophs and as an important tool for the study of gonadotroph physiology.
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Matson, Christine, and B. T. Donovan. "Acute effects of GnRF-induced gonadotrophin secretion upon ovarian steroid secretion in the ferret." Acta Endocrinologica 111, no. 3 (March 1986): 373–77. http://dx.doi.org/10.1530/acta.0.1110373.
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Abstract. The effects of an increase in endogenous gonadotrophin secretion on the production of oestradiol, progesterone, androstenedione and testosterone by the ovaries of anaesthetized anoestrous and oestrous ferrets were followed. Gonadotrophin secretion was enhanced by the injection of gonadotrophin releasing factor (GnRF), and serial blood samples were collected over 9 h for hormone assay. Thyrotrophic hormone releasing factor (TRF) or acetic acid were injected for control purposes. The plasma content of oestradiol in oestrous females was significantly higher than during anoestrus, but secretion of this steroid was not increased by any means. The plasma concentration of progesterone in anoestrous females was significantly higher than during oestrus. It was increased by GnRF in anoestrous ferrets and less markedly in oestrous females. The plasma concentration of androstenedione was raised by GnRF to a greater extent during anoestrus than during oestrus. Testosterone was present in higher concentration in the plasma during anoestrus than during oestrus, and the level was increased by GnRF administration. These findings indicate that the ovaries of the anoestrous ferret secrete significant quantities of steroid hormones, and that they respond readily to gonadotrophic hormone.
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Brooks, J., and A. S. McNeilly. "Regulation of gonadotrophin-releasing hormone receptor mRNA expression in the sheep." Journal of Endocrinology 143, no. 1 (October 1994): 175–82. http://dx.doi.org/10.1677/joe.0.1430175.
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Abstract To investigate the regulation of the sheep gonadotrophin-releasing hormone receptor (GnRH-R) gene expression, two different treatment regimes were used. Experiment 1 examined the effects of twice daily injections of ovine follicular fluid (oFF, 15 ml s.c.) as a source of inhibin, and daily GnRH antagonist injections (Nal-Glu.HOAc, 2 mg s.c.) on days 9–12 of the oestrous cycle. Luteolysis was induced on day 12 with prostaglandin (PG) and the ewes killed at two different stages; day 12 (luteal) and 18 h after PG injection. Experiment 2 examined the effect of a single injection of oestradiol benzoate (100 μg i.m.) 18 h before death in luteal phase ewes and ewes chronically implanted with the GnRH agonist, buserelin. In both experiments, pituitaries were removed at death for determination of pituitary GnRH binding, LH content and levels of GnRH-R and LHβ mRNA. In addition in experiment 1, follicles ≥2·5 mm were dissected from the ovaries for determination of oestradiol content. In experiment 1, oFF treatment during the luteal phase completely inhibited follicle oestradiol production but was without effect on the other parameters measured. After cessation of oFF treatment and induction of luteolysis, a significant (P<0·05) increase in plasma LH occurred but the normal follicular increase in both GnRH-R mRNA levels and GnRH binding seen in control ewes was prevented. GnRH antagonist treatment alone or in combination with oFF also inhibited follicle oestradiol production, prevented the increase in GnRH-R mRNA, completely inhibited GnRH binding and significantly decreased LHβ mRNA levels. Pituitary LH content was unaffected by any treatment. In experiment 2, oestradiol treatment did not affect GnRH-R mRNA levels, GnRH binding, LHβ mRNA or pituitary LH content in luteal phase ewes, whilst chronic GnRH agonist treatment acted to decrease these parameters dramatically. A single injection of oestradiol in the GnRH agonist treated ewes significantly (P<0·05) increased GnRH-R mRNA levels and completely restored GnRH binding to luteal levels, without any effect on LHβ mRNA or pituitary LH content. These results suggest that the control of GnRH receptor expression in the sheep is directly related to oestradiol and not to the action of GnRH itself. Journal of Endocrinology (1994) 143, 175–182
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Ferris, J. K., M. T. Tse, D. K. Hamson, M. D. Taves, C. Ma, N. McGuire, L. Arckens, et al. "Neuronal Gonadotrophin-Releasing Hormone (GnRH) and Astrocytic Gonadotrophin Inhibitory Hormone (GnIH) Immunoreactivity in the Adult Rat Hippocampus." Journal of Neuroendocrinology 27, no. 10 (September 21, 2015): 772–86. http://dx.doi.org/10.1111/jne.12307.
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Sun, Fei, Dun Qing Yan, Gong Li Zhang, Jin Yu, and En Nian Xiao. "Miscarriage Prevention Tea Affects Plasma β-Endorphin Concentrations in Women with Early Threatened Abortions." American Journal of Chinese Medicine 27, no. 02 (January 1999): 277–82. http://dx.doi.org/10.1142/s0192415x99000318.
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Twenty threatened abortive patients in the 7-8th week of gestation were treated with a classical miscarriage prevention tea (Shou-Tai-Tang) combined with psychological consultation. All of the patients had a history of unexplained recurrent abortions. This treatment succeeded in sixteen out of 20 patients. The plasma concentrations of ß-endorphin (ß-EP), gonadotrophin releasing hormone (GnRH), human chorionic gonadotrophin (hCG), and progesterone (P4) were measured by radioimmunoassay before and after treatment. Comparied to control subjects, ß-EP levels were significantly higher, while GnRH, hCG, and P4 were lower than before treatment. Concentrations of these peptides/hormones returned to normal ranges after successful treatment.
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Khurshid, S., G. F. Weinbauer, and E. Nieschlag. "Effects of administration of testosterone and gonadotrophin-releasing hormone (GnRH) antagonist on basal and GnRH-stimulated gonadotrophin secretion in orchidectomized monkeys." Journal of Endocrinology 129, no. 3 (June 1991): 363–70. http://dx.doi.org/10.1677/joe.0.1290363.
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ABSTRACT The aim of the present investigation was to investigate the effects of testosterone on basal and gonadotrophin-releasing hormone (GnRH)-stimulated gonadotrophin secretion in the presence and absence of a GnRH antagonist in a non-human primate model (Macaca fascicularis). Orchidectomized animals were used in order to avoid interference by testicular products other than testosterone involved in gonadotrophin feedback. Concomitant and delayed administration of testosterone at doses that provided serum levels either within the intact range (study 1) or markedly above that range (study 2) did not influence the suppression of basal gonadotrophin release induced by the GnRH antagonist during a 15-day period. To assess the possible effects of testosterone treatment at the pituitary level (study 3) GnRH stimulation tests (500 μg) were performed before and on days 8 and 15 of treatment with high-dose testosterone and GnRH antagonist alone or in combination. Testosterone alone abolished the gonadotrophin responses to exogenous GnRH observed under pretreatment conditions. With GnRH antagonist alone, an increased responsiveness (P <0·05) to GnRH was seen on day 8 and a similar response compared with pretreatment on day 15. Following combined treatment with GnRH antagonist and testosterone, GnRH-induced gonadotrophin secretion was consistently lower compared with that after GnRH antagonist alone (P <0·05), but was increased compared with that after testosterone alone (P<0·05). Thus, in the presence of a GnRH antagonist the feedback action of testosterone on LH and FSH was diminished. The present work in GnRH antagonist-treated orchidectomized monkeys demonstrates that (I) unlike in rats, testosterone fails to stimulate FSH secretion selectively, (II) the negative feedback action of testosterone on GnRH-stimulated LH and FSH secretion is altered in the presence of a GnRH antagonist and (III) GnRH antagonists induce a transient period of increased responsiveness of gonadotrophic hormone release to exogenous GnRH. The observation that a GnRH antagonist reduced the feedback effects of testosterone suggests that testosterone action on pituitary gonadotrophin release, at least in part, is mediated via hypothalamic GnRH. Journal of Endocrinology (1991) 129, 363–370
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Cheng, Kwai Wa, and Peter CK Leung. "The expression, regulation and signal transduction pathways of the mammalian gonadotropin-releasing hormone receptor." Canadian Journal of Physiology and Pharmacology 78, no. 12 (December 1, 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.