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1
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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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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Burger, L. L., D. J. Haisenleder, A. C. Dalkin, and J. C. Marshall. "Regulation of gonadotropin subunit gene transcription." Journal of Molecular Endocrinology 33, no. 3 (December 2004): 559–84. http://dx.doi.org/10.1677/jme.1.01600.
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Reproductive function in mammals is regulated by the pituitary gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH and FSH are secreted by the gonadotrope cell and act on the gonad in a sequential and synergistic manner to initiate sexual maturation and maintain cyclic reproductive function. The synthesis and secretion of LH and FSH are regulated mainly by the pulsatile release of the hypothalamic decapeptide hormone gonadotropin-releasing hormone (GnRH). The control of differential LH and FSH synthesis and secretion is complex and involves the interplay between the gonads, hypothalamus and pituitary. In this review, the transcriptional regulation of the gonadotropin subunit genes is discussed in a physiologic setting, and we aimed to examine the mechanisms that drive those changes.
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Rebers, Frank E. M., Peter T. Bosma, Wytske van Dijk, Henk J. T. Goos, and Rüdiger W. Schulz. "GnRH stimulates LH release directly via inositol phosphate and indirectly via cAMP in African catfish." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 6 (June 1, 2000): R1572—R1578. http://dx.doi.org/10.1152/ajpregu.2000.278.6.r1572.
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In African catfish, two gonadotropin-releasing hormone (GnRH) peptides have been identified: chicken GnRH (cGnRH)-II and catfish GnRH (cfGnRH). The GnRH receptors on pituitary cells producing gonadotropic hormone signal through inositol phosphate (IP) elevation followed by increases in intracellular calcium concentration ([Ca2+]i). In primary pituitary cell cultures of male African catfish, both cGnRH-II and cfGnRH dose dependently elevated IP accumulation, [Ca2+]i, and the release of the luteinizing hormone (LH)-like gonadotropin. In all cases, cGnRH-II was more potent than cfGnRH. The GnRH-stimulated LH release was not associated with elevated cAMP levels, and forskolin-induced cAMP elevation had no effect on LH release. With the use of pituitary tissue fragments, however, cAMP was elevated by GnRH, and forskolin was able to stimulate LH secretion. Incubating these fragments with antibodies against cfGnRH abolished the forskolin-induced LH release but did not compromise the forskolin-induced cAMP elevation. This suggests that cfGnRH-containing nerve terminals are present in pituitary tissue fragments and release cfGnRH via cAMP signaling on GnRH stimulation, whereas the GnRH receptors on gonadotrophs use IP/[Ca2+]i to stimulate the release of LH.
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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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Ceccatelli, S., A. L. Hulting, X. Zhang, L. Gustafsson, M. Villar, and T. Hökfelt. "Nitric oxide synthase in the rat anterior pituitary gland and the role of nitric oxide in regulation of luteinizing hormone secretion." Proceedings of the National Academy of Sciences 90, no. 23 (December 1, 1993): 11292–96. http://dx.doi.org/10.1073/pnas.90.23.11292.
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By using immunohistochemistry and in situ hybridization, we have demonstrated that the nitric oxide (NO)-synthesizing enzyme NO synthase is present in gonadotrophs and in folliculo-stellate cells of the anterior pituitary gland of male and female rats. A marked increase in levels of NO synthase protein and mRNA was observed after gonadectomy. In vitro studies on dispersed anterior pituitary cells suggest that NO inhibits gonadotropin-releasing-hormone-stimulated luteinizing hormone release. An inhibitory effect of NO has also been shown on growth-hormone-releasing-hormone-stimulated release of growth hormone [Kato, M. (1992) Endocrinology 131, 2133-2138]. Thus these findings support a dual mechanism for NO in the control of anterior pituitary hormone secretion, an autocrine mediation of luteinizing hormone release on gonadotrophs, and a paracrine effect on growth hormone secretion involving folliculo-stellate cells closely related to somatotrophs. We speculate that NO may participate in producing the pulsatile secretion patterns of these two pituitary hormones.
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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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Daftary, Shabrine S., and Andrea C. Gore. "IGF-1 in the Brain as a Regulator of Reproductive Neuroendocrine Function." Experimental Biology and Medicine 230, no. 5 (May 2005): 292–306. http://dx.doi.org/10.1177/153537020523000503.
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Given the close relationship among neuroendocrine systems, it Is likely that there may be common signals that coordinate the acquisition of adult reproductive function with other homeo-static processes. In this review, we focus on central nervous system insulin-like growth factor-1 (IGF-1) as a signal controlling reproductive function, with possible links to somatic growth, particularly during puberty. In vertebrates, the appropriate neurosecretion of the decapeptide gonadotropin-releas-ing hormone (GnRH) plays a critical role in the progression of puberty. Gonadotropin-releasing hormone is released in pulses from neuroterminals in the median eminence (ME), and each GnRH pulse triggers the production of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). These pituitary hormones in turn stimulate the synthesis and release of sex steroids by the gonads. Any factor that affects GnRH or gonadotropin pulsatility is important for puberty and reproductive function and, among these factors, the neurotrophic factor IGF-1 is a strong candidate. Although IGF-1 is most commonly studied as the tertiary peripheral hormone in the somatotropic axis via its synthesis in the liver, IGF-1 Is also synthesIzed in the brain, within neurons and glia. In neuroendocrine brain regions, central IGF-1 plays roles in the regulation of neuroendocrine functions, including direct actions on GnRH neurons. Moreover, GnRH neurons themselves co-express IGF-1 and the IGF-1 receptor, and this expression is developmentally regulated. Here, we examine the role of IGF-1 acting in the hypothalamus as a critical link between reproductive and other neuroendocrine functions.
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Blaakaer, Jan, Henning Djursing, Ulla Hørding, Paul Bennett, Kim Toftager-Larsen, Johannes E. Bock, and Paul E. Lebech. "The pituitary-gonadal axis in women with benign or malignant ovarian tumors." Acta Endocrinologica 127, no. 2 (August 1992): 127–30. http://dx.doi.org/10.1530/acta.0.1270127.
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The serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), human chorionic gonadotropin (hCG), estradiol, progesterone, androstenedione, testosterone (total and free) and dehydroepiandrosterone sulphate (DHEAS) were investigated prior to surgery in 24 postmenopausal women with benign and 28 postmenopausal women with malignant epithelial ovarian tumors. The serum concentrations of hormones were compared with those of 28 healthy, postmenopausal, age-matched controls. Significantly lower serum FSH levels were demonstrated in women with malignant tumors. No significant differences were found between the groups regarding the serum LH levels. The hCG levels were low in all groups. Regarding progesterone and estradiol levels, low postmenopausal steroid levels were found in all groups examined and no significant differences were demonstrated within the groups. No significant correlations between the levels of estradiol and FSH or progesterone and LH were demonstrated. To exclude a central depression of gonadotropin release mediated by the dopaminergic system we examined the thyroid stimulating hormone (TSH) and prolactin. No differences were found between the groups regarding TSH and prolactin levels. A possible relationship between other hormones/factors produced by the tumor and exerting a negative feedback, either centrally or directly, on the gonadotropin release remains to be investigated. A change in biological activity in the gonadotropins might explain the present findings.
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Zhou, Hong, Xinyan Wang, Wendy K. W. Ko, and Anderson O. L. Wong. "Evidence for a Novel Intrapituitary Autocrine/Paracrine Feedback Loop Regulating Growth Hormone Synthesis and Secretion in Grass Carp Pituitary Cells by Functional Interactions between Gonadotrophs and Somatotrophs." Endocrinology 145, no. 12 (December 1, 2004): 5548–59. http://dx.doi.org/10.1210/en.2004-0362.
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Abstract Gonadotropin (GTH) and GH released from the pituitary are known to interact at multiple levels to modulate the functions of the gonadotrophic and somatotrophic axes. However, their interactions at the pituitary level have not been fully characterized. In this study, autocrine/paracrine regulation of GH synthesis and secretion by local interactions between gonadotrophs and somatotrophs was examined using grass carp pituitary cells as a cell model. Exogenous GTH and GH induced GH release and GH mRNA expression in carp pituitary cells. Removal of endogenous GTH and GH by immunoneutralization with GTH and GH antisera, respectively, suppressed GH release, GH production, and GH mRNA levels. GH antiserum also blocked the stimulatory effects of exogenous GTH on GH release and GH mRNA levels. In reciprocal experiments, GH release and GH mRNA expression induced by exogenous GH was significantly reduced by GTH antiserum. In addition, exogenous GH was found to be inhibitory to basal GTH release and treatment with GH antiserum elevated GTH secretion at low doses but suppressed GTH production at high doses. These results suggest that local interactions between gonadotrophs and somatotrophs may form an intrapituitary feedback loop to regulate GH release and synthesis. In this model, GTH released from gonadotrophs induces GH release and GH production in neighboring somatotrophs. GH secreted maintains somatotroph sensitivity to GTH stimulation, and at the same time, inhibits basal GTH release in gonadotrophs. This feedback loop may represent a novel mechanism regulating GH release and synthesis in lower vertebrates.
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Millar, RP, PJ Wormald, and RC Milton. "Stimulation of gonadotropin release by a non-GnRH peptide sequence of the GnRH precursor." Science 232, no. 4746 (April 4, 1986): 68–70. http://dx.doi.org/10.1126/science.3082009.
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The human gonadotropin-releasing hormone (GnRH) precursor comprises the GnRH sequence followed by an extension of 59 amino acids. Basic amino acid residues in the carboxyl terminal extension may represent sites of processing to biologically active peptides. A synthetic peptide comprising the first 13 amino acids (H X Asp-Ala-Glu-Asn-Leu-Ile-Asp-Ser-Phe-Gln-Glu-Ile-Val X OH) of the 59-amino acid peptide was found to stimulate the release of gonadotropic hormones from human and baboon anterior pituitary cells in culture. The peptide did not affect thyrotropin or prolactin secretion. A GnRH antagonist did not inhibit gonadotropin stimulation by the peptide, and the peptide did not compete with GnRH for GnRH pituitary receptors, indicating that the action of the peptide is independent of the GnRH receptor. The GnRH precursor contains two distinct peptide sequences capable of stimulating gonadotropin release from human and baboon pituitary cells.
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Vanecek, J., and D. C. Klein. "Melatonin inhibition of GnRH-induced LH release from neonatal rat gonadotroph: involvement of Ca2+ not cAMP." American Journal of Physiology-Endocrinology and Metabolism 269, no. 1 (July 1, 1995): E85—E90. http://dx.doi.org/10.1152/ajpendo.1995.269.1.e85.
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Melatonin inhibits gonadotropin-releasing hormone-induced release of luteinizing hormone (LH) from the neonatal rat gonadotrophs. The second messenger involved is not known, although there are several candidates, including adenosine 3',5'-cyclic monophosphate (cAMP) and intracellular free Ca2+. The present study addresses the question of which second messenger mediates melatonin inhibition of LH release. We found that the effect of melatonin was not prevented by cAMP protagonists, including 8-bromo-cAMP, dibutyryl cAMP, 3-isobutyl-1-methylxanthine, and forskolin. However, treatments that enhanced Ca2+ influx masked the effects of melatonin, and treatments that blocked Ca2+ influx mimicked the effects of melatonin. Moreover, melatonin decreased K(+)-induced LH release, which is dependent on Ca2+ influx but did not block release of LH due to thapsigargin-induced mobilization of Ca2+ from intracellular stores. These findings indicate that melatonin inhibits gonadotropin-releasing hormone-induced LH release, primarily through an action involving inhibition of Ca2+ influx, and that cAMP does not seem to be involved in this effect of melatonin.
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Jayasena, Channa N., Gurjinder M. K. Nijher, Alexander N. Comninos, Ali Abbara, Adam Januszewki, Meriel L. Vaal, Labosshy Sriskandarajah, et al. "The Effects of Kisspeptin-10 on Reproductive Hormone Release Show Sexual Dimorphism in Humans." Journal of Clinical Endocrinology & Metabolism 96, no. 12 (December 1, 2011): E1963—E1972. http://dx.doi.org/10.1210/jc.2011-1408.
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Abstract Background: Kisspeptin peptides are critical in human reproductive physiology and are potential therapies for infertility. Kisspeptin-10 stimulates gonadotropin release in both male and female rodents. However, few studies have investigated the effects of kisspeptin-10 on gonadotropin release in humans, and none have investigated the effect in women. If kisspeptin is to be useful for treating reproductive disease, its effects in both men and women must be established. Aim: To compare the effects of kisspeptin-10 administration on reproductive hormone release in healthy men and women. Methods: Intravenous bolus kisspeptin-10 was administered to men and women (n = 4–5 per group). Subcutaneous bolus and iv infusion of kisspeptin-10 was also administered to female women (n = 4–5 per group). Circulating reproductive hormones were measured. Results: In healthy men, serum LH and FSH were elevated after iv bolus kisspeptin-10, at doses as low as 0.3 and 1.0 nmol/kg, respectively. In healthy women during the follicular phase of the menstrual cycle, no alterations in serum gonadotropins were observed after iv bolus, sc bolus, or iv infusion of kisspeptin-10 at maximal doses of 10 nmol/kg, 32 nmol/kg, and 720pmol/kg/min, respectively. In women during the preovulatory phase, serum LH and FSH were elevated after iv bolus kisspeptin-10 (10 nmol/kg). Conclusion: Kisspeptin-10 stimulates gonadotropin release in men as well as women during the preovulatory phase of menstrual cycle but fails to stimulate gonadotropin release in women during the follicular phase. The sexual dimorphism of the responsiveness of healthy men and women to kisspeptin-10 administration has important clinical implications for the potential of kisspeptin-10 to treat disorders of reproduction.
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Crowley, W. R. "Toward Multifactorial Hypothalamic Regulation of Anterior Pituitary Hormone Secretion." Physiology 14, no. 2 (April 1999): 54–58. http://dx.doi.org/10.1152/physiologyonline.1999.14.2.54.
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The hypothalamus regulates the secretion of anterior pituitary hormones via release of releasing hormones into the hypophysial portal vasculature. Additional neuromessengers act at the pituitary to modulate responses to the hypothalamic hormones. For example, neuropeptide Y enhances the effect of gonadotropin-releasing hormone and the response to the prolactin-inhibiting hormone dopamine.
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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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Allaerts, Wilfried, Ans MI Tijssen, Pieter HM Jeucken, Hemmo A. Drexhage, and Jurrien de Koning. "Influence of folliculo-stellate cells on biphasic luteinizing hormone secretion response to gonadotropin-releasing hormone in rat pituitary cell aggregates." European Journal of Endocrinology 130, no. 5 (May 1994): 530–39. http://dx.doi.org/10.1530/eje.0.1300530.
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Allaerts W, Tijssen AMI, Jeucken PHM, Drexhage HA, de Koning J. Influence of folliculo-stellate cells on biphasic luteinizing hormone secretion response to gonadotropin-releasing hormone in rat pituitary cell aggregates. Eur J Endocrinol 1994;130:530–9. ISSN 0804–4643 Anterior pituitary cells cultured as three-dimensional cell aggregates and incubated with gonadotropin-releasing hormone (GnRH) show a biphasic pattern of luteinizing hormone (LH) release when steroid-free bovine follicle fluid is added to the culture medium. Initially, the GnRH-induced LH release is low (lag-phase response), but LH release increases during further incubations with GnRH (primed-state response). Also, in aggregates of dispersed cells from long-term ovariectomized rats cultured for 2 days in the presence of 1% bovine follicle fluid, a low initial LH responsiveness to GnRH could be restored. Cycloheximide was found to block the induction of the primed state, indicating the protein synthesis dependency of GnRH self-priming. In aggregates from gonadotroph-enriched cell populations obtained by velocity sedimentation in a bovine serum albumin gradient, addition of 1% bovine follicle fluid to the culture medium also restored a biphasic pattern of GnRH-induced LH release. However, co-culturing the gonadotroph-enriched cell aggregates with a folliculo-stellate (FS) cell-enriched population resulted in the attenuation of the differences in LH secretion rate between early and late responses to GnRH. The present example of the attenuation by folliculo-stellate cells of pituitary hormone secretion responses demonstrates that the cells regulate the cellular processes leading to a priming of the LH response to GnRH, rather than interfering with the access of GnRH to its receptor in gonadotrophs. Finally, it was found that stimulation of the adenylate cyclase enzyme with maximal effective doses of forskolin counteracted the inhibitory effect of bovine follicle fluid on the initial LH response to GnRH, but did not completely abolish the biphasic pattern of LH release. It is concluded that coupling to the adenylate cyclase enzyme is presumably involved in the LH surge inhibiting feedback action on the pituitary cells, but also other messenger pathways and intercellular interactions between pituitary cells may play a role in establishing a biphasic LH release at the pituitary level following GnRH administration. W Allaerts, Dept. of Immunology, Erasmus University Rotterdam, PO Box 1738, 3000 DR Rotterdam, The Netherlands
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Jamaluddin, Md, Partha P. Banerjee, Pulak R. Manna, and Samir Bhattacharya. "Requirement of extracellular calcium in fish pituitary gonadotropin release by gonadotropin hormone-releasing hormone." General and Comparative Endocrinology 74, no. 2 (May 1989): 190–98. http://dx.doi.org/10.1016/0016-6480(89)90212-8.
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Son, You Lee, Takayoshi Ubuka, Robert P. Millar, Haruhiko Kanasaki, and Kazuyoshi Tsutsui. "Gonadotropin-Inhibitory Hormone Inhibits GnRH-Induced Gonadotropin Subunit Gene Transcriptions by Inhibiting AC/cAMP/PKA-Dependent ERK Pathway in LβT2 Cells." Endocrinology 153, no. 5 (February 28, 2012): 2332–43. http://dx.doi.org/10.1210/en.2011-1904.
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A neuropeptide that directly inhibits gonadotropin secretion from the pituitary was discovered in quail and named gonadotropin-inhibitory hormone (GnIH). The presence and functional roles of GnIH orthologs, RF-amide-related peptides (RFRP), that possess a common C-terminal LPXRF-amide (X = L or Q) motif have also been demonstrated in mammals. GnIH orthologs inhibit gonadotropin synthesis and release by acting on pituitary gonadotropes and GnRH neurons in the hypothalamus via its receptor (GnIH receptor). It is becoming increasingly clear that GnIH is an important hypothalamic neuropeptide controlling reproduction, but the detailed signaling pathway mediating the inhibitory effect of GnIH on target cells is still unknown. In the present study, we investigated the pathway of GnIH cell signaling and its possible interaction with GnRH signaling using a mouse gonadotrope cell line, LβT2. First, we demonstrated the expression of GnIH receptor mRNA in LβT2 cells by RT-PCR. We then examined the inhibitory effects of mouse GnIH orthologs [mouse RFRP (mRFRP)] on GnRH-induced cell signaling events. We showed that mRFRP effectively inhibited GnRH-induced cAMP signaling by using a cAMP-sensitive reporter system and measuring cAMP levels, indicating that mRFRP function as an inhibitor of adenylate cyclase. We further showed that mRFRP inhibited GnRH-stimulated ERK phosphorylation, and this effect was mediated by the inhibition of the protein kinase A pathway. Finally, we demonstrated that mRFRP inhibited GnRH-stimulated gonadotropin subunit gene transcriptions and also LH release. Taken together, the results indicate that mRFRP function as GnIH to inhibit GnRH-induced gonadotropin subunit gene transcriptions by inhibiting adenylate cyclase/cAMP/protein kinase A-dependent ERK activation in LβT2 cells.
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Yu, W. H., S. Karanth, C. A. Mastronardi, S. Sealfon, C. Dean, W. L. Dees, and S. M. McCann. "Lamprey GnRH-III Acts on Its Putative Receptor via Nitric Oxide to Release Follicle-Stimulating Hormone Specifically." Experimental Biology and Medicine 227, no. 9 (October 2002): 786–93. http://dx.doi.org/10.1177/153537020222700910.
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Lamprey gonadotropin-releasing hormone-III (I-GnRH-III), the putative follicle-stimulating hormone (FSH)-releasing factor (FSHRF), exerts a preferential FSH-releasing activity in rats both in vitro and in vivo. To test the hypothesis that I-GnRH-III acts on its own receptors to stimulate gonadotropin release, the functional activity of this peptide at mammalian (m) leutinizing hormone (LH)RH receptors transfected to COS cells was tested. I-GnRH-III activated m-LHRH receptors only at a minimal effective concentration (MEC) of 10–6 M, whereas m-LHRH was active at a MEC of 10–9 M, at least 1,000 times less than that required for I-GnRH-III. In 4-day monolayer cultured cells, I-GnRH-III was similarly extremely weak in releasing either LH or FSH, and, in fact, it released LH at a lower concentration (10–7 M) than that required for FSH release (10–6 M). In this assay, m-LHRH released both FSH and LH significantly at the lowest concentration tested (10–10 M). On the other hand, I-GnRH-III had a high potency to selectively release FSH and not LH from hemipituitaries of male rats. The results suggest that the cultured cells were devoid of FSHRF receptors, thereby resulting in a pattern of FSH and LH release caused by the LHRH receptor. On the other hand, the putative FSH-releasing factor receptor accounts for the selective FSH release by I-GnRH-III when tested on hemipituitaries. Removal of calcium from the medium plus the addition of EGTA, a calcium chelator, suppressed the release of gonadotropins induced by either I-GnRH-III or LHRH, indicating that calcium is required for the action of either peptide. Previous results showed that sodium nitroprusside, a releaser of nitric oxide (NO), causes the release of both FSH and LH from hemipituitaries incubated in vitro. In the present experiments, a competitive inhibitor of NO synthase, L-NG-monomethyl-l-arginine (300 μM) blocked the action of I-GnRH-III or partially purified FSHRF. The results indicate that I-GnRH-III and FSHRF act on putative FSHRF receptors by a calcium-dependent NO pathway.
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Rodríguez Gabilondo, Adrian, Liz Hernández Pérez, and Rebeca Martínez Rodríguez. "Hormonal and neuroendocrine control of reproductive function in teleost fish." Bionatura 3, no. 3 (August 15, 2021): 2122–33. http://dx.doi.org/10.21931/rb/2021.06.02.35.
Full textAbstract:
Reproduction is one of the important physiological events for the maintenance of the species. Hormonal and neuroendocrine regulation of teleost requires multiple and complex interactions along the hypothalamic-pituitary-gonad (HPG) axis. Within this axis, gonadotropin-releasing hormone (GnRH) regulates the synthesis and release of gonadotropins, follicle-stimulating hormone (FSH), and luteinizing hormone (LH). Steroidogenesis drives reproduction function in which the development and differentiation of gonads. In recent years, new neuropeptides have become the focus of reproductive physiology research as they are involved in the different regulatory mechanisms of these species' growth, metabolism, and reproduction. However, especially in fish, the role of these neuropeptides in the control of reproductive function is not well studied. The study of hormonal and neuroendocrine events that regulate reproduction is crucial for the development and success of aquaculture.
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Kile, J. P., and M. S. Amoss. "Role of Ca2+ and Na+ on luteinizing hormone release from the calf pituitary." American Journal of Physiology-Endocrinology and Metabolism 255, no. 4 (October 1, 1988): E469—E474. http://dx.doi.org/10.1152/ajpendo.1988.255.4.e469.
Full textAbstract:
It has been proposed that gonadotropin-releasing hormone (GnRH) stimulates Ca2+ entry by activation of voltage-independent, receptor-mediated Ca2+ channels in the rat gonadotroph. Little work has been done on the role of calcium in GnRH-induced luteinizing hormone (LH) release in species other than the rat. Therefore, this study was done to compare the effects of agents that alter Ca2+ or Na+ entry on LH release from calf anterior pituitary primary cells in culture. GnRH (100 ng/ml), Ca2+ ionophore A23187 (2.5 microM), and the depolarizing agent ouabain (0.1-10 microM) all produced significant increases (P less than 0.05) in LH release; these effects were significantly reduced when the cells were preincubated with the organic Ca2+ channel blockers nifedipine (1-10 microM) and verapamil (1-10 microM) and with Co2+ (0.01-1 mM). The effect of ouabain was inhibited by tetrodotoxin (TTX; 1-10 nM) as well as by nifedipine at 0.1-10 microM. In contrast to its effect on rat pituitary LH release, TTX significantly inhibited GnRH-stimulated LH release at 1-100 nM. These results suggest that GnRH-induced LH release may employ Ca2+ as a second messenger in bovine gonadotrophs and support recent speculation that GnRH-induced Ca2+ mobilization may in part be voltage dependent.
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Levy, Tally, and Zion Ben-Rafael. "Pharmacokinetics of gonadotropin therapy." Reproductive Medicine Review 5, no. 1 (March 1996): 13–35. http://dx.doi.org/10.1017/s0962279900001216.
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Ovulation is the result of an integrated action of the hypothalamus, pituitary and ovaries. During the process, gonadal steroids, peptides and growth factors are produced and influence the synthesis and release of gonadotropin-releasing hormone (GnRH), follicle stimulating hormone (FSH) and luteinizing hormone (LH). These latter compounds play a crucial role in folliculogenesis and are frequently used in the management of infertility.
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Lim, Stefan, Min Luo, Mingshi Koh, Meng Yang, Mohammed Nizam bin Abdul Kadir, Jing Hui Tan, Zhiyong Ye, Wen Wang, and Philippa Melamed. "Distinct Mechanisms Involving Diverse Histone Deacetylases Repress Expression of the Two Gonadotropin β-Subunit Genes in Immature Gonadotropes, and Their Actions Are Overcome by Gonadotropin-Releasing Hormone." Molecular and Cellular Biology 27, no. 11 (March 19, 2007): 4105–20. http://dx.doi.org/10.1128/mcb.00248-07.
Full textAbstract:
ABSTRACT The gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are produced in the embryonic pituitary in response to delivery of the hypothalamic gonadotropin releasing hormone (GnRH). GnRH has a pivotal role in reestablishing gonadotropin levels at puberty in primates, and for many species with extended reproductive cycles, these are reinitiated in response to central nervous system-induced GnRH release. Thus, a clear role is evident for GnRH in overcoming repression of these genes. Although the mechanisms through which GnRH actively stimulates LH and FSH β-subunit (FSHβ) gene transcription have been described in some detail, there is currently no information on how GnRH overcomes repression in order to terminate reproductively inactive stages. We show here that GnRH overcomes histone deacetylase (HDAC)-mediated repression of the gonadotropin β-subunit genes in immature gonadotropes. The repressive factors associated with each of these genes comprise distinct sets of HDACs and corepressors which allow for differentially regulated derepression of these two genes, produced in the same cell by the same regulatory hormone. We find that GnRH activation of calcium/calmodulin-dependent protein kinase I (CaMKI) plays a crucial role in the derepression of the FSHβ gene involving phosphorylation of several class IIa HDACs associated with both the FSHβ and Nur77 genes, and we propose a model for the mechanisms involved. In contrast, derepression of the LH β-subunit gene is not CaMK dependent. This demonstration of HDAC-mediated repression of these genes could explain the temporal shut-down of reproductive function at certain periods of the life cycle, which can easily be reversed by the actions of the hypothalamic regulatory hormone.
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Trudeau, V. L., D. Spanswick, E. J. Fraser, K. Larivière, D. Crump, S. Chiu, M. MacMillan, and R. W. Schulz. "The role of amino acid neurotransmitters in the regulation of pituitary gonadotropin release in fish." Biochemistry and Cell Biology 78, no. 3 (April 2, 2000): 241–59. http://dx.doi.org/10.1139/o99-075.
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Both glutamate and γ-aminobutyric acid (GABA) are involved in pituitary hormone release in fish. Glutamate serves 2 purposes, both as a neurotransmitter and as a precursor for GABA synthesis. Glutamate can be catabolized to GABA by the actions of 2 distinct but related enzymes, glutamate decarboxylase 65 (GAD65) and GAD67. They derive from 2 different genes that likely arose from an early gene duplication prior to the emergence of teleosts more than 400 million years ago. There is good evidence for the involvement of GABA in luteinizing hormone (LH) release in fish. The mechanism of GABA action to stimulate LH release appears to be a combination of effects on GnRH release, potentiation of gonadotropin hormone-releasing hormone (GnRH) action, and in some cases directly at the LH cell. These actions appear to be dependent on such factors as sex or sex steroid levels, and there may also be species differences. Nevertheless, the stimulatory effects of GABA on LH are present in at least 4 fish species. In contrast, convincing data for the inhibitory effects of GABA on LH release have only been observed in 1 fish species. The sites and mechanisms of action of amino acid neurotransmitters on LH release have yet to be fully characterized. Both N-methyl-D-aspartic acid (NMDA) and S-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) type glutamate receptors are likely to have important roles. We suggest that it is a receptor similar to the GABAA type which mediates the effects of GABA on LH release in fish, at least partially acting on the GnRH neuron, but likely directly acting at the gonadotroph as well. GABA may also be involved in regulating the release of other pituitary hormones in fish, namely follicle stimulating hormone (FSH = GTH-I), prolactin, and growth hormone. Based on the findings described in this review, a working model for the involvement of glutamate and GABA in the regulation of LH release in teleost fish is proposed. Key words: glutamate, GABA, luteinizing hormone, muscimol, patch clamp electrophysiology, reproduction, fish.
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Bourne, G. A., and D. M. Baldwin. "Evidence for cAMP as a mediator of gonadotropin secretion from female pituitaries." American Journal of Physiology-Endocrinology and Metabolism 253, no. 3 (September 1, 1987): E290—E295. http://dx.doi.org/10.1152/ajpendo.1987.253.3.e290.
Full textAbstract:
Sodium flufenamate, which inhibited gonadotropin-releasing hormone (GnRH)-stimulated increases in adenosine 3',5'-cyclic monophosphate (cAMP), was used to evaluate the potential role of cAMP as a mediator of GnRH-stimulated gonadotropin secretion. Quartered pituitaries from diestrous II female rats were perifused at 37 degrees C, and sequential effluent fractions were collected every 10 min. Administration of GnRH resulted in a characteristic biphasic response for both luteinizing hormone (LH) and follicle-stimulating hormone (FSH), whereas 5 microM cycloheximide inhibited the secondary augmented responses (phase II) of both hormones. Infusions of 0.1 mM flufenamate inhibited GnRH-stimulated gonadotropin secretion in a manner similar to that of cycloheximide, whereas the administration of 5 mM dibutyryl cAMP in combination with GnRH and flufenamate resulted in the restoration of LH and FSH secretion. The dibutyryl cAMP-restored response appeared to be protein synthesis dependent and specific for cAMP. These results suggest that although the cyclic nucleotide is not involved in the acute release of LH and FSH, it does appear to play a pivotal but indirect role in phase II release of the hormones, by effects involving the stimulation of de novo protein synthesis.
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de Castro Assis, Luiz Henrique, Rafael Henrique de Nóbrega, Nuria Esther Gómez-González, Jan Bogerd, and Rüdiger Winfried Schulz. "Estrogen-induced inhibition of spermatogenesis in zebrafish is largely reversed by androgen." Journal of Molecular Endocrinology 60, no. 4 (May 2018): 273–84. http://dx.doi.org/10.1530/jme-17-0177.
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The hormonal regulation of spermatogenesis involves both gonadotropins and steroid hormones. Long-term in vivo exposure of adult zebrafish to estrogen impaired spermatogenesis associated with an androgen insufficiency, possibly induced by inhibiting gonadotropin release. Using this experimental model, we investigated if androgen treatment could enhance spermatogenesis, while maintaining the inhibition of gonadotropin release through continued estrogen exposure. Moreover, we also exposed animals to androgen alone, in order to examine androgen effects in the absence of estrogen-induced gonadotropin inhibition. Estrogen exposure depleted type B spermatogonia, meiotic and postmeiotic germ cells from the adult testis, but promoted the proliferation of type A undifferentiated spermatogonia, which accumulated in the testis. This change in germ cell composition was accompanied by reduced mRNA levels of those growth factors (e.g. insl3 and igf3) expressed by testicular somatic cells and known to stimulate spermatogonial differentiation in zebrafish. Additional androgen (11-ketoandrostenedione, which is converted to 11-ketotestosterone) treatment in vivo reversed most of the effects of estrogen exposure on spermatogenesis while insl3 and igf3 transcript levels remained suppressed. When androgen treatment was given alone, it promoted the production of haploid cells at the expense of spermatogonia, and increased transcript levels of some growth factor and hormone receptor genes, but not those of insl3 or igf3. We conclude that estrogen exposure efficiently inhibits spermatogenesis because it induces androgen insufficiency and suppresses gonadotropin-regulated growth factors known to stimulate germ cell differentiation. Moreover, our results suggest that androgens and the growth factors Insl3 and Igf3 stimulate spermatogenesis via independent pathways.
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Herbison, Allan E. "The Gonadotropin-Releasing Hormone Pulse Generator." Endocrinology 159, no. 11 (September 28, 2018): 3723–36. http://dx.doi.org/10.1210/en.2018-00653.
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Abstract The pulsatile release of GnRH and LH secretion is essential for fertility in all mammals. Pulses of LH occur approximately every hour in follicular-phase females and every 2 to 3 hours in luteal-phase females and males. Many studies over the last 50 years have sought to identify the nature and mechanism of the “GnRH pulse generator” responsible for pulsatile LH release. This review examines the characteristics of pulsatile hormone release and summarizes investigations that have led to our present understanding of the GnRH pulse generator. There is presently little compelling evidence for an intrinsic mechanism of pulse generation involving interactions between GnRH neuron cell bodies. Rather, data support the presence of an extrinsic pulse generator located within the arcuate nucleus, and attention has focused on the kisspeptin neurons and their projections to GnRH neuron dendrons concentrated around the median eminence. Sufficient evidence has been gathered in rodents to conclude that a subpopulation of arcuate kisspeptin neurons is, indeed, the GnRH pulse generator. Findings in other species are generally compatible with this view and suggest that arcuate/infundibular kisspeptin neurons represent the mammalian GnRH pulse generator. With hindsight, it is likely that past arcuate nucleus multiunit activity recordings have been from kisspeptin neurons. Despite advances in identifying the cells forming the pulse generator, almost nothing is known about their mechanisms of synchronicity and the afferent hormonal and transmitter modulation required to establish the normal patterns of LH pulsatility in mammals.
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Krsmanovic, Lazar Z., Stanko S. Stojilkovic, and Kevin J. Catt. "Pulsatile gonadotropin-releasing hormone release and its regulation." Trends in Endocrinology & Metabolism 7, no. 2 (March 1996): 56–59. http://dx.doi.org/10.1016/1043-2760(96)00007-0.
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Blum, J. Joseph, Michael C. Reed, Jo Ann Janovick, and P. Michael Conn. "A mathematical model quantifying GnRH-induced LH secretion from gonadotropes." American Journal of Physiology-Endocrinology and Metabolism 278, no. 2 (February 1, 2000): E263—E272. http://dx.doi.org/10.1152/ajpendo.2000.278.2.e263.
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A mathematical model is developed to investigate the rate of release of luteinizing hormone (LH) from pituitary gonadotropes in response to short pulses of gonadotropin-releasing hormone (GnRH). The model includes binding of the hormone to its receptor, dimerization, interaction with a G protein, production of inositol 1,4,5-trisphosphate, release of Ca2+ from the endoplasmic reticulum, entrance of Ca2+ into the cytosol via voltage-gated membrane channels, pumping of Ca2+ out of the cytosol via membrane and endoplasmic reticulum pumps, and release of LH. Cytosolic Ca2+ dynamics are simplified (i.e., oscillations are not included in the model), and it is assumed that there is only one pool of releasable LH. Despite these and other simplifications, the model explains the qualitative features of LH release in response to GnRH pulses of various durations and different concentrations in the presence and absence of external Ca2+.
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Barnes, Maria J., Karen Lapanowski, Jose A. Rafols, David M. Lawson, and Joseph C. Dunbar. "Chronic Nitric Oxide Deficiency is Associated with Altered Leutinizing Hormone and Follicle-Stimulating Hormone Release in Ovariectomized Rats1." Experimental Biology and Medicine 227, no. 9 (October 2002): 817–22. http://dx.doi.org/10.1177/153537020222700915.
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Nitric oxide (NO) synthase (NOS) has been found in the gonadotrophs and folliculo-stellate cells of the anterior pituitary. Previous observations from our laboratory suggest that NO may play a role in regulating gonadotropin secretion. Because estrogen secretion by the ovary can influence gonadotropin secretion, we investigated the hypothesis that chronic in vivo NO deficiency has a direct estrogen-independent effect on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Chronic NO deficiency was induced by adding an NOS inhibitor, N-nitro-L-arginine (L-NNA, 0.6 g/l) to the drinking water of ovariectomized (OVX) rats. The control OVX rats were untreated. After 6–8 weeks, the animals were sacrificed, and the pituitaries were removed and perfused continuously for 4 hr in the presence of pulsatile gonadotropin-releasing hormone (GnRH, 500 ng/pulse) every 30 min. S-Nitroso-l-acetyl penicillamine (SNAP, an NO donor, 0.1 mM) or l-nitro-arginine methyl ester (L-NAME, an NOS inhibitor, 0.1 mM) was added to the media and perfusate samples were collected at 10-min intervals. GnRH-stimulated LH and FSH levels were significantly lower in pituitaries from OVX/NO-deficient pituitaries compared with pituitaries from the OVX control group. The addition of SNAP significantly decreased LH and FSH secretion by pituitaries from OVX control animals, but significantly increased their secretion by pituitaries from the OVX/NO-deficient animals. L-NAME also suppressed LH and FSH secretion by pituitaries from the OVX control animals and stimulated their release by pituitaries from the NO-deficient/OVX animals. Immunohisto-chemistry of frontal sections through the hypothalamus demonstrated that OVX/NO deficiency is associated with increased GnRH in the median eminence. We conclude that NO has a chronic stimulatory effect on LH and FSH release and the subsequent altered secretory responsiveness to NO agonist or antagonist is the result of chronic NO suppression.
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Kraak, Glen Van Der, Edward M. Donaldson, and John P. Chang. "Dopamine involvement in the regulation of gonadotropin secretion in coho salmon." Canadian Journal of Zoology 64, no. 6 (June 1, 1986): 1245–48. http://dx.doi.org/10.1139/z86-185.
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The effects of intraperitoneal injections of [D-Ala6,Pro9-N-ethylamide]-luteinizing hormone-releasing hormone (LHRH-A) and pimozide, a dopamine receptor antagonist, on plasma gonadotropin levels and ovulation in coho salmon were investigated. Both LHRH-A (0.02 mg/kg body weight) and pimozide (10 mg/kg body weight) stimulate gonadotropin secretion, with LHRH-A causing a more rapid onset of gonadotropin release and a higher magnitude increase in plasma gonadotropin levels than pimozide. Pimozide caused a marked potentiation of the gonadotropin release response to LHRH-A. Injections of LHRH-A alone and in combination with pimozide were effective means of inducing ovulation, whereas pimozide alone was ineffective. These data support the concept that dopamine participates in the regulation of gonadotropin secretion in teleosts and suggest that dopamine has a minor role in the regulation of ovulatory gonadotropin changes in coho salmon compared with cyprinids.
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Bourne, G. A., and D. M. Baldwin. "Evidence for cAMP as a mediator of gonadotropin secretion from male pituitaries." American Journal of Physiology-Endocrinology and Metabolism 253, no. 3 (September 1, 1987): E296—E299. http://dx.doi.org/10.1152/ajpendo.1987.253.3.e296.
Full textAbstract:
The purpose of this study was to use sodium flufenamate, a compound that inhibits gonadotropin-releasing hormone (GnRH)-stimulated adenosine 3',5'-cyclic monophosphate (cAMP) production in the pituitary, to evaluate the potential role of cAMP as a mediator of GnRH-stimulated gonadotropin secretion from male pituitaries. Quartered male pituitaries were perifused at 37 degrees C and sequential effluent fractions collected every 10 min. Infusions of GnRH resulted in a twofold increase in luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion. Cycloheximide, 5 microM, completely inhibited the GnRH-stimulated LH and FSH secretion. Infusions of 0.1 mM flufenamate had similar effects on gonadotropin secretion as cycloheximide, whereas the administration of 5 mM dibutyryl cAMP in combination with GnRH and flufenamate restored the secretory responses of both hormones. The flufenamate-inhibited GnRH stimulated LH and FSH release, which was restored by DBcAMP and appeared to be protein synthesis dependent and specific for cAMP. These results suggest an indirect role for cAMP as a mediator of gonadotropin secretion from male pituitaries. However, in contrast to female pituitaries, the secretion of these hormones from male pituitaries is completely dependent on cAMP and de novo protein synthesis.
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Lewy, Hadas, Zvi Naor, and Israel E. Ashkenazi. "Rhythmicity of luteinizing hormone secretion expressed in vitro." European Journal of Endocrinology 135, no. 4 (October 1996): 455–63. http://dx.doi.org/10.1530/eje.0.1350455.
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Lewy H, Naor Z, Ashkenazi IE. Rhythmicity of luteinizing hormone secretion expressed in vitro. Eur J Endocrinol 1996;135:455–63. ISSN 0804–4643 In the present study we explored the possibility that the pituitary functions as an autonomous clock and is capable of generating rhythms of luteinizing hormone (LH) release independently of hypothalamic control. Pituitaries from estrous or diestrous day 1 female mice were perifused separately with Medium-199. Effluent samples were collected at 10-min intervals and assayed for LH levels. Fourier analysis and curve-fit analysis served to elucidate the presence of prominent periods whose significance was then determined by best-fit cosinor. The latter method was used to determine additional parameters for the significant rhythm. All perifused pituitaries exhibited LH release patterns that were composed of significantly long ultradian rhythms (approximately 16 and 8 h, p < 0.001). Continuous stimulation with gonadotropin-releasing hormone (GnRH) or estradiol did not alter the periods of the observed rhythms but affected other rhythm parameters. Gonadotropin-releasing hormone increased the mesor of the rhythm and estradiol increased the amplitude. The results indicate that pituitary gonadotropes are capable of producing rhythms of LH release for a long duration in vitro, in the absence of hypothalamic control. Both GnRH and estradiol affect different rhythm parameters but do not change the periods of these rhythms. Israel E Ashkenazi, Department of Human Genetics, Sackler School of Medicine, Tel Aviv University, Tel Aviv 69978, Israel
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Ma, Yunyong, Scott A. Juntti, Caroline K. Hu, John R. Huguenard, and Russell D. Fernald. "Electrical synapses connect a network of gonadotropin releasing hormone neurons in a cichlid fish." Proceedings of the National Academy of Sciences 112, no. 12 (March 9, 2015): 3805–10. http://dx.doi.org/10.1073/pnas.1421851112.
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Initiating and regulating vertebrate reproduction requires pulsatile release of gonadotropin-releasing hormone (GnRH1) from the hypothalamus. Coordinated GnRH1 release, not simply elevated absolute levels, effects the release of pituitary gonadotropins that drive steroid production in the gonads. However, the mechanisms underlying synchronization of GnRH1 neurons are unknown. Control of synchronicity by gap junctions between GnRH1 neurons has been proposed but not previously found. We recorded simultaneously from pairs of transgenically labeled GnRH1 neurons in adult male Astatotilapia burtoni cichlid fish. We report that GnRH1 neurons are strongly and uniformly interconnected by electrical synapses that can drive spiking in connected cells and can be reversibly blocked by meclofenamic acid. Our results suggest that electrical synapses could promote coordinated spike firing in a cellular assemblage of GnRH1 neurons to produce the pulsatile output necessary for activation of the pituitary and reproduction.
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Christian, M. S., and N. A. Trenton. "Evaluation of thyroid function in neonatal and adult rats: The neglected endocrine mode of action." Pure and Applied Chemistry 75, no. 11-12 (January 1, 2003): 2055–68. http://dx.doi.org/10.1351/pac200375112055.
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Although known to regulate growth and development, cellular metabolism, the use of oxygen, and basal metabolic rate, thyroid hormones have been only minimally evaluated in neonatal rodents at critical times of development. Despite some modulation of metabolic rate by other hormones, such as testosterone, growth hormone, and norepinephrine, 3,5,3'-triiodothyronine (T3) and 3,5,3',5'-tetraiodothyronine (T4) are the most important metabolic rate modulators. Endpoints used for thyroid function assessment in neonatal and adult rats include thyroid-stimulating hormone (TSH), T3, and T4 levels and histopathology. In rodents, decreased serum levels of T3 and T4 and increased serum TSH levels, with sustained release of TSH and resultant follicular cell hypertrophy/hyperplasia, are typical hormonal and histopathological findings attributable to compounds altering thyroid function. Hypothyroidism early in the neonatal period can affect reproductive endpoints in both male and female rats, with the critical period of exposure being the first two weeks postnatal. Hypothyroidism has been shown to reduce gonadotrophin levels and delay pubertal spermatogenesis in male rats and to block gonadotropin-induced first ovulation in immature female rats by decreasing FSH and luteinizing hormone (LH) serum concentrations. Inclusion of evaluations of TSH, T3, and T4 assays in multigeneration and developmental neurotoxicity protocols may assist in risk assessments.
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Tejada, Francisco, Asunción Cremades, Manuel Avilés, Maria T. Castells, and Rafael Peñafiel. "Hypokalemia alters sex hormone and gonadotropin levels: evidence that FSH may be required for luteinization." American Journal of Physiology-Endocrinology and Metabolism 275, no. 6 (December 1, 1998): E1037—E1045. http://dx.doi.org/10.1152/ajpendo.1998.275.6.e1037.
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Hypokalemia produced different effects on steroid sex hormone concentrations in plasma and ovary in the mouse. Estradiol levels were slightly increased, whereas circulating progesterone was markedly decreased in all estrous periods. The preovulatory surge of gonadotropins and the secondary surge of follicle-stimulating hormone (FSH) at estrus were also decreased, but basal levels of both gonadotropins were unaffected. Supplementation with luteinizing hormone (LH), FSH, or gonadotropin-releasing hormone (GnRH) at proestrus rapidly normalized plasma and ovarian progesterone levels at this stage of the estrous cycle. Plasma progesterone levels at diestrus were restored only by combined treatment, at the periovulatory stage, with LH and FSH or GnRH but not by LH or FSH alone. The results demonstrate a lack of steroidogenic activity in the corpus luteum of the potassium-deficient mice and, furthermore, that FSH plays an important role in luteinization in the hypokalemic mice. We conclude that alteration of the transcellular potassium gradient may affect the regulation of the periovulatory surge of gonadotropins and progesterone secretion, probably by altering the release of GnRH from the hypothalamus. In addition, the results suggest that FSH may play a certain role as a luteotropic hormone in mice.
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Naor, Zvi, Henry N. Jabbour, Michal Naidich, Adam J. Pawson, Kevin Morgan, Sharon Battersby, Michael R. Millar, Pamela Brown, and Robert P. Millar. "Reciprocal Cross Talk between Gonadotropin-Releasing Hormone (GnRH) and Prostaglandin Receptors Regulates GnRH Receptor Expression and Differential Gonadotropin Secretion." Molecular Endocrinology 21, no. 2 (February 1, 2007): 524–37. http://dx.doi.org/10.1210/me.2006-0253.
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Abstract The asynchronous secretion of gonadotrope LH and FSH under the control of GnRH is crucial for ovarian cyclicity but the underlying mechanism is not fully resolved. Because prostaglandins (PG) are autocrine regulators in many tissues, we determined whether they have this role in gonadotropes. We first demonstrated that GnRH stimulates PG synthesis by induction of cyclooxygenase-2, via the protein kinase C/c-Src/phosphatidylinositol 3′-kinase/MAPK pathway in the LβT2 gonadotrope cell line. We then demonstrated that PGF2α and PGI2, but not PGE2 inhibited GnRH receptor expression by inhibition of phosphoinositide turnover. PGF2α, but not PGI2 or PGE2, reduced GnRH-induction of LHβ gene expression, but not the α-gonadotropin subunit or the FSHβ subunit genes. The prostanoid receptors EP1, EP2, FP, and IP were expressed in rat gonadotropes. Incubations of rat pituitaries with PGF2α, but not PGI2 or PGE2, inhibited GnRH-induced LH secretion, whereas the cyclooxygenase inhibitor, indomethacin, stimulated GnRH-induced LH secretion. None of these treatments had any effect on GnRH-induced FSH secretion. The findings have thus elaborated a novel GnRH signaling pathway mediated by PGF2α-FP and PGI2-IP, which acts through an autocrine/paracrine modality to limit autoregulation of the GnRH receptor and differentially inhibit LH and FSH release. These findings provide a mechanism for asynchronous LH and FSH secretions and suggest the use of combination therapies of GnRH and prostanoid analogs to treat infertility, diseases with unbalanced LH and FSH secretion and in hormone-dependent diseases such as prostatic cancer.
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Kotsuji, Fumikazu, Takeshi Aso, Naoyuki Kamitani, and Toshiro Tominaga. "The synthesis and release of gonadotropins in response to gonadotropin-releasing hormone of the rat anterior pituitary gland during weight reduction." Acta Endocrinologica 122, no. 5 (May 1990): 628–32. http://dx.doi.org/10.1530/acta.0.1220628.
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Abstract. It is well recognized that weight reduction produces the suppression of serum LH but not FSH level in rodents. In order to clarify the mechanism by which the discrepancy between LH and FSH levels is brought about, the influence of weight loss on the pituitary function was explored using female rats. The changes of the pituitary response to GnRH and the basal secretion of gonadotropins with progressive weight loss were investigated by in vitro short-term incubation of the pituitary gland after prolonged weight loss in female Wistar rats. On the first day of diestrous and until day 14 of the diet, GnRH induced LH and FSH release from the pituitary and a decrease in pituitary content of them, but the total amount of gonadotropin in culture medium and pituitary tissue was not affected. On day 30 of the diet, the decrease in pituitary content disappeared. On day 60 LH release disappeared, whereas pituitary FSH and the total amount of gonadotropins were increased by GnRH. Non-stimulated FSH but not LH secretion per mg of pituitary was augmented during dieting. The data indicate that pituitary responsiveness to GnRH and non-stimulated FSH release were modified by weight loss: the LH-releasing action of GmRH was diminished, the gonadotropin-synthesizing action of GnRH was augmented, and non-stimulated FSH release was increased.
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Weber, GM, JF Powell, M. Park, WH Fischer, AG Craig, JE Rivier, U. Nanakorn, et al. "Evidence that gonadotropin-releasing hormone (GnRH) functions as a prolactin-releasing factor in a teleost fish (Oreochromis mossambicus) and primary structures for three native GnRH molecules." Journal of Endocrinology 155, no. 1 (October 1, 1997): 121–32. http://dx.doi.org/10.1677/joe.0.1550121.
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Three forms of gonadotropin-releasing hormone (GnRH) are isolated and identified here by chemical sequence analysis for one species of tilapia, Oreochromis niloticus, and by HPLC elution position for a second species of tilapia, O. mossambicus. Of the three GnRH forms in O. mossambicus, chicken GnRH-II (cGnRH-II) and sea bream GnRH (sbGnRH) are present in greater abundance in the brain and pituitary than salmon GnRH (sGnRH). These three native forms of GnRH are shown to stimulate the release of prolactin (PRL) from the rostral pars distalis (RPD) of the pituitary of O. mossambicus in vitro with the following order of potency: cGnRH-II > sGnRH > sbGnRH. In addition, a mammalian GnRH analog stimulated the release of PRL from the pituitary RPD incubated in either iso-osmotic (320 mosmol/l) or hyperosmotic (355 mosmol/l) medium, the latter normally inhibiting PRL release. The response of the pituitary RPD to GnRH was augmented by co-incubation with testosterone or 17 beta-estradiol. The effects of GnRH on PRL release appear to be direct effects on PRL cells because the RPD of tilapia contains a nearly homogeneous mass of PRL cells without intermixing of gonadotrophs. Our data suggest that GnRH plays a broad role in fish, depending on the species, by affecting not only gonadotropins and growth hormone, but also PRL.
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Armstrong, Jennifer, and Gwen V. Childs. "Differential Expression of c-fos In Vitro by All Anterior Pituitary Cell Types During the Estrous Cycle: Enhanced Expression by Luteinizing Hormone but Not by Follicle-stimulating Hormone Cells." Journal of Histochemistry & Cytochemistry 45, no. 6 (June 1997): 785–94. http://dx.doi.org/10.1177/002215549704500603.
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C-fos expression appears in some activated cell types. Because of dynamic changes in gonadotropes during the estrous cycle, this study was initiated to determine if fos might be expressed in gonadotropes before any period of activation. We detected c-fos and pituitary antigens in dissociated anterior pituitary cells by dual-labeling immunocy-tochemistry. The highest percentages of cells with fos protein were found in proestrous rat populations. In diestrous and proestrous populations, dual labeling showed that 6–9% of pituitary cells contained fos with adrenocorticotropin, thyroid-stimulating hormone, prolactin, or growth hormone antigens. In contrast, only 0.8–3% contained fos with luteinizing hormone (LH) or follicle-stimulating hormone (FSH) antigens. We then tested the hypothesis that gonadotropes might increase fos expression earlier in the cycle. In populations from metestrous rats, c-fos labeling was found in 45% of LH cells compared to only 23% of LH cells in the proestrous group. This suggests that proportionately more LH cells are being activated to produce fos early in the cycle. Perhaps fos is used in translation of LHβ antigens or gonadotropin-releasing hormone (GnRH) receptor mRNAs. In contrast, less than 1% of all pituitary cells expressed fos with FSH at all stages of the cycle (only 6–12% of FSH cells). This differential expression suggests one mechanism behind the regulation of non-parallel storage and release of gonadotropin antigens.
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Negrón, Ariel L., Guiqin Yu, Ulrich Boehm, and Maricedes Acosta-Martínez. "Targeted Deletion of PTEN in Kisspeptin Cells Results in Brain Region- and Sex-Specific Effects on Kisspeptin Expression and Gonadotropin Release." International Journal of Molecular Sciences 21, no. 6 (March 19, 2020): 2107. http://dx.doi.org/10.3390/ijms21062107.
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Kisspeptin-expressing neurons in the anteroventral periventricular nucleus (AVPV) and the arcuate nucleus (ARC) of the hypothalamus relay hormonal and metabolic information to gonadotropin-releasing hormone neurons, which in turn regulate pituitary and gonadal function. Phosphatase and tensin homolog (PTEN) blocks phosphatidylinositol 3-kinase (PI3K), a signaling pathway utilized by peripheral factors to transmit their signals. However, whether PTEN signaling in kisspeptin neurons helps to integrate peripheral hormonal cues to regulate gonadotropin release is unknown. To address this question, we generated mice with a kisspeptin cell-specific deletion of Pten (Kiss-PTEN KO), and first assessed kisspeptin protein expression and gonadotropin release in these animals. Kiss-PTEN KO mice displayed a profound sex and region-specific kisspeptin neuron hyperthrophy. We detected both kisspeptin neuron hyperthrophy as well as increased kisspeptin fiber densities in the AVPV and ARC of Kiss-PTEN KO females and in the ARC of Kiss-PTEN KO males. Moreover, Kiss-PTEN KO mice showed a reduced gonadotropin release in response to gonadectomy. We also found a hyperactivation of mTOR, a downstream PI3K target and central regulator of cell metabolism, in the AVPV and ARC of Kiss-PTEN KO females but not males. Fasting, known to inhibit hypothalamic kisspeptin expression and luteinizing hormone levels, failed to induce these changes in Kiss-PTEN KO females. We conclude that PTEN signaling regulates kisspeptin protein synthesis in both sexes and that its role as a metabolic signaling molecule in kisspeptin neurons is sex-specific.
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Zwart, Alexander D., Randall J. Urban, William D. Odell, and Johannes D. Veldhuis. "Contrasts in the gonadotropin-releasing hormone dose–response relationships for luteinizing hormone, follicle-stimulating hormone and α-subunit release in young versus older men: appraisal with high-specificity immunoradiometric assay and deconvolution analysis." European Journal of Endocrinology 135, no. 4 (October 1996): 399–406. http://dx.doi.org/10.1530/eje.0.1350399.
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Zwart AD, Urban RJ, Odell WD, Veldhuis JD. Contrasts in the gonadotropin-releasing hormone dose–response relationships for luteinizing hormone, follicle-stimulating hormone and α-subunit release in young versus older men: appraisal with high-specificity immunoradiometric assay and deconvolution analysis. Eur J Endocrinol 1996:135:399–406. ISSN 0804–4643 The secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) is regulated by gonadotropin-releasing hormone (GnRH). As men age, mean serum concentrations of immunoreactive gonadotropic hormones tend to increase, while serum testosterone concentrations tend to decline. To evaluate age-related changes in gonadotroph cell function, we have assessed the dose-dependent secretory responses of immunoreactive LH, FSH and α-subunit to saline versus five doses of GnRH in older and young men. Ten older men, mean age 66 years (range 61–78), and nine young men, mean age 26 years (range 22–30), received iv bolus injections of GnRH (range 10–100 μg) in randomized order every 2 h. except that the 100-μg dose was always given last. Blood samples for immunoradiometric assays of serum LH, FSH and α-subunit concentrations were obtained every 10 min for a total of 12 h, which included a 2-h preinjection baseline. Deconvolution analysis was performed to estimate gonadotropin and α-subunit secretory burst mass, amplitude and duration, as well as endogenous LH, FSH and α-subunit half-lives. The mean (± sem) baseline 2-h serum FSH (IU/l) concentration was higher in older than younger men (5.9 ± 0.8 vs 3.8 ± 0.5, p < 0.05). The mean 2-h serum LH concentrations after GnRH were significantly higher than corresponding values in young men at GnRH doses of 25, 50 and 75 μg, and in the case of FSH at GnRH doses of 10 and 25 μg. Non-linear curve-fitting of these dose–response relationships revealed that the calculated maximal mean 2-h serum LH concentration response (IU/l) was higher in older than young men following GnRH stimulation: 15.4 (13.5–16.2) vs 10.8 (8.7–12.1) (95% confidence interval). The maximal mean 2-h serum FSH concentration response (IU/l) was also significantly higher in older men: 11.9 (10.2–13.1) versus 8.6 (7.2–9.6). Maximal α-subunit responses (μg/l) were similarly increased in the older cohort: 1.16 (0.99–1.25) vs 0.83 (0.71–0.91). The incremental LH (p < 0.05) and FSH (p < 0.01) secretory burst mass from 10 to 25 μg GnRH was significantly greater in older than younger men. The LH and FSH half-lives and second component α-subunit half-lives were similar in older and young men. In addition, secretory burst durations were invariant of age. In contrast, by non-linear curve-fitting, the calculated mass of LH secreted was higher in older men at 13.5 (11.8–15) vs 10.6 (9.2–11.7) IU/l of distribution volume (p < 0.05) for the maximal absolute mass and 11.3 (9.5–12.7) vs 7.4 (6.0–8.4) IU/l (p < 0.05) for the maximal incremental mass of LH secreted after GnRH. The estimated maximal mass of FSH secreted after GnRH also was higher in older men: 4.6 (3.4–5.5) vs 3.2 (2.9–3.4) IU/l (p < 0.01). Finally, calculated maximal GnRH-stimulated α-subunit secretory burst mass was statistically greater in older individuals: 2.3 (1.8–2.5) vs 1.6 (1.4–1.8) μg/l. In contrast, half-maximally effective GnRH doses were not different in the two age groups. We conclude that older men show significantly increased maximal and incremental gonadotropin release due to amplified secretory burst mass in response to escalating doses of GnRH with no evident differences in LH, FSH, or α-subunit half-lives or secretory burst durations. Increased gonadotroph responsiveness may be due to diminished gonadal hormone negative feedback or primary alterations in the hypothalamo-pituitary unit with aging. Johannes D Veldhuis, Division of Endocrinology and Metabolism, Box 202, Department of Internal Medicine, University of Virginia Health Sciences Center, Charlottesville, VA 22908, USA
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Moenter, S. M., R. M. Brand, A. R. Midgley, and F. J. Karsch. "Dynamics of gonadotropin-releasing hormone release during a pulse." Endocrinology 130, no. 1 (January 1992): 503–10. http://dx.doi.org/10.1210/endo.130.1.1727719.
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Skinner, Donal C., Alain Caraty, and Neil P. Evans. "Does Gonadotropin-Releasing Hormone in the Cerebrospinal Fluid Modulate Luteinizing Hormone Release?" Neuroendocrinology 67, no. 1 (1998): 37–44. http://dx.doi.org/10.1159/000054296.
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BEGGS, MICHAEL J., and WILLIAM L. MILLER. "Gonadotropin-Releasing Hormone- Stimulated Luteinizing Hormone (LH) Release from Ovine Gonadotrophs in Culture Is Separate from Phorbol Ester-Stimulated LH Release*." Endocrinology 124, no. 2 (February 1989): 667–74. http://dx.doi.org/10.1210/endo-124-2-667.
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Chan, John S. D., Jie-Ying Deng, Anoop K. Brar, Nabil G. Seidah, and Michel Chrétien. "Inhibition of release of a novel pituitary polypeptide, 7B2, follicle-stimulating hormone, and luteinizing hormone from rat anterior pituitary cells in vitro by human β-inhibin." Canadian Journal of Physiology and Pharmacology 64, no. 9 (September 1, 1986): 1259–62. http://dx.doi.org/10.1139/y86-212.
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We have recently purified a novel pituitary polypeptide designated 7B2. By raising polyclonal antibodies to a synthetic 7B2 fragment in rabbits, we have developed a sensitive and specific radioimmunoassay for this novel polypeptide, and it has been used for the study of the release of immunoreactive 7B2 from rat anterior pituitary cells in vitro. In addition, immunocytochemical study shows that 7B2 is present in the gonadotropin cells of rat anterior pituitary. The aim of the present studies is to investigate the effect of human β-inhibin, testosterone, and combined testosterone plus human β-inhibin on the induced release of immunoreactive 7B2, follicle-stimulating hormone (FSH), and luteinizing hormone (LH) in rat anterior pituitary cell culture in vitro. Our results show that both human β-inhibin and testosterone effectively suppress the stimulatory effect of luteinizing hormone-releasing hormone (LHRH) on immunoreactive 7B2, FSH, and LH release. The present data indicate that the regulation of secretion of 7B2 and pituitary gonadotropins may be under a similar type of feedback mechanism.
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Krsmanovic, Lazar Z., Antonio J. Martinez-Fuentes, Krishan K. Arora, Nadia Mores, Carlos E. Navarro, Hao-Chia Chen, Stanko S. Stojilkovic, and Kevin J. Catt. "Autocrine Regulation of Gonadotropin-Releasing Hormone Secretion in Cultured Hypothalamic Neurons." Endocrinology 140, no. 3 (March 1, 1999): 1423–31. http://dx.doi.org/10.1210/endo.140.3.6588.
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Abstract Episodic hormone secretion is a characteristic feature of the hypothalamo-pituitary-gonadal system, in which the profile of gonadotropin release from pituitary gonadotrophs reflects the pulsatile secretory activity of GnRH-producing neurons in the hypothalamus. Pulsatile release of GnRH is also evident in vitro during perifusion of immortalized GnRH neurons (GT1–7 cells) and cultured fetal hypothalamic cells, which continue to produce bioactive GnRH for up to 2 months. Such cultures, as well as hypothalamic tissue from adult rats, express GnRH receptors as evidenced by the presence of high-affinity GnRH binding sites and GnRH receptor transcripts. Furthermore, individual GnRH neurons coexpress GnRH and GnRH receptors as revealed by double immunostaining of hypothalamic cultures. In static cultures of hypothalamic neurons and GT1–7 cells, treatment with the GnRH receptor antagonist, [d-pGlu1, d-Phe2, d-Trp3,6]GnRH caused a prominent increase in GnRH release. In perifused hypothalamic cells and GT1–7 cells, treatment with the GnRH receptor agonist, des-Gly10-[d-Ala6]GnRH N-ethylamide, reduced the frequency and increased the amplitude of pulsatile GnRH release, as previously observed in GT1–7 cells. In contrast, exposure to the GnRH antagonist analogs abolished pulsatile secretion and caused a sustained and progressive increase in GnRH release. These findings have demonstrated that GnRH receptors are expressed in hypothalamic GnRH neurons, and that receptor activation is required for pulsatile GnRH release in vitro. The effects of GnRH agonist and antagonist analogs on neuropeptide release are consistent with the operation of an ultrashort-loop autocrine feedback mechanism that exerts both positive and negative actions that are necessary for the integrated control of GnRH secretion from the hypothalamus.
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Sanford, Lee M., and Bernard Robaire. "Interaction of season and estradiol in the regulation of gonadotropin secretion in the adult ram." Canadian Journal of Physiology and Pharmacology 68, no. 2 (February 1, 1990): 150–56. http://dx.doi.org/10.1139/y90-024.
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The effects of season and estradiol on the secretion of gonadotropic hormones in adult Dorset × Leicester × Suffolk rams were studied. Control groups of intact and castrate rams, and castrate rams given estradiol replacement (~ 11.5 pg/mL) via polydimethylsiloxane capsules (sc) were assessed for 1 year, beginning in August. Mean concentrations of luteinizing hormone (LH), follicle-stimulating hormone (FSH), and prolactin (PRL) were determined every 2 weeks for all three groups of rams and measurements of testosterone concentration and scrotal circumference were taken on the intact rams. Pulsatile LH release and the LH response to a 2-μg dose (iv) of gonadotropin-releasing hormone (GnRH) were assessed for all rams when the testes of intact rams were redeveloped (late October), regressed (early February, late April), and redeveloping (early August). Season directly affected LH-pulse amplitude, which increased only in the control castrate rams between February and April. In October, LH-pulse frequency was the same in both groups of castrate rams, while in April, frequency in the estradiol-treated castrate rams was suppressed to intact ram values. Pituitary responsiveness to exogenous GnRH did not change throughout the year in either of the castrate groups, but along with LH-pulse amplitude, it was increased in August in the intact rams. Although FSH secretion was 14-fold higher in the control castrate rams than in the intact rams, seasonal-directional changes in mean concentration were similar. FSH concentration in the estradiol-treated castrate rams was stable throughout the year. PRL secretion never differed between the control castrate and intact rams but was enhanced in the estradiol-treated castrate rams, particularly during long days.Key words: season, estradiol, gonadotropins, adult ram.
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Gidley-Baird, A. A., B. M. White, J. Hau, and O. M. Poulsen. "Initiation and control of ovulation in the mouse luteal phases. Effects of gonadotropins and gonadotropin releasing hormone." Acta Endocrinologica 113, no. 4 (December 1986): 576–81. http://dx.doi.org/10.1530/acta.0.1130576.
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Abstract. The aim of the present study was to examine the induction of ovulation during pregnancy, pseudopregnancy, and suckling-delayed pregnancy in mice using exogenous gonadotropins. The present results demonstrate that there are mature follicles in the ovary which can be induced to ovulate with administration of either exogenous human chorionic gonadotropin (hCG) or luteinizing hormone (LH) during pregnancy (Days 1–12) and pseudopregnancy (Days 4–8) in the mouse. hCG was relatively ineffective in initiating ovulation during suckling-delayed pregnancy, and hCG could not induce ovulation on Days 3–6 in any animals, suggesting that follicular growth is not continuous during suckling-delayed pregnancy in the mouse. Ovulation occurred in pregnant and pseudopregnant mice following injection of gonadotropin releasing hormone (GnRH) in a gelatin delay vehicle. Injection of GnRH in saline did not initiate ovulation in pregnant or pseudopregnant mice. A large release of LH was shown to occur following injection of GnRH in gelatin, but no release occurred after the same dose of GnRH in saline. In conclusion, the experiments demonstrate the existence of mature follicles during murine pregnancy and pseudopregnancy, and the lack of inductable follicles during suckling-delayed pregnancy.