Relevant bibliographies by topics / Gonadotropin release hormone

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Gonadotropin release hormone'

Author: Grafiati
Published: 4 June 2021
Last updated: 13 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Gonadotropin release hormone.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Gonadotropin release hormone"

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
4

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
5

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.

Full text
Abstract:
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
APA, Harvard, Vancouver, ISO, and other styles
6

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
7

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
8

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
9

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Gonadotropin release hormone"

1

MacConell, Leigh Anne. "The regulation of gonadotropin-releasing hormone biosynthesis and release by activin A /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9904817.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Borsari, Rodrigo. "Expressão gênica do leiomioma uterino em mulheres no período reprodutivo após tratamento com análogo agonista do GnRH." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-30012009-160208/.

Full text
Abstract:
OBJETIVO: Identificar os genes diferencialmente expressos entre os leiomiomas uterinos de pacientes em idade reprodutiva, tratadas ou não com análogo do GnRH e confirmar os resultados obtidos para genes selecionados por técnica de PCR em tempo real. PACIENTES E MÉTODOS: Foi colhida amostra do maior nódulo de leiomioma uterino de 89 pacientes negras, idade entre 20 e 45 anos, com indicação cirúrgica de miomectomia. Dessas, 38 receberam análogo do GnRH previamente a cirurgia (Grupo A) e 51 foram submetidas a cirurgia sem tratamento prévio (Grupo B). Dentro de cada grupo foram selecionadas 10 pacientes nulíparas, com maior nódulo acima de 3,0 cm, volume uterino acima de 300 cc. e amostras colhidas na fase lútea no Grupo B. INTERVENÇÃO: 5 amostras de cada grupo foram analisadas por técnica de microarray e posteriormente genes diferencialmente expressos foram analisados por técnica de PCR em tempo real em 10 pacientes de cada grupo. RESULTADOS: Do total de 47.000 seqüências da plataforma Affymetrix, representando em torno de 38.500 genes humanos já caracterizados, resultou na expressão diferencial de 174 genes, sendo 70 super-expressos (33 com função conhecida) e 104 subexpressos (65 com função conhecida) em amostras do Grupo A (Tratado) comparativamente ao Grupo B (Não-Tratado). Os genes super-expressos CYR 61, EGR 1 e SULF 2 e o sub-expresso, WIF 1 foram confirmados por PCR em tempo real, enquanto o gene HMGN1 não teve confirmação da sua super-expressão após PCR em tempo real. CONCLUSÕES: Há alteração da expressão gênica de leiomioma uterino de mulheres submetidas a tratamento com análogo de GnRH em relação às não tratadas. O número de genes sub-expressos é o dobro dos super-expressos e 80% das alterações detectadas pela técnica de microarray foram confirmadas por PCR em tempo real.
OBJECTIVE: To identify the genes differentially expressed between the uterine leiomyomas of patients in reproductive age, treat or not treated with GnRH analogue and confirm the results for genes selected by real time PCR. METHODS: It was harvested sample of the largest lump of uterine leiomyoma of 89 black patients, aged between 20 and 45 years, with details of surgical miomectomia. Of these, 38 patients received GnRH analogue prior to surgery (Group A) and 51 were undergoing surgery without prior treatment (Group B). Within each group were selected 10 patients nulliparous, with higher nodule over 3.0 cm, uterine volume over 300 cc. and samples taken during lutea in Group B. INTERVENTION: 5 samples from each group were analyzed by microarray, and then differentially expressed genes were analyzed by real time PCR on 10 patients in each group. RESULTS: Of the 47,000 sequences of the platform used, representing around 38,500 human genes already characterized, resulted in differential expression of 174 genes, with 70 genes up regulated (33 genes with known function) and 104 down regulated (65 genes with known function) in samples of Group A (Treaty) compared to Group B (Non-Treaty). The up regulated genes CYR 61, EGR 1 and SULF 2 and down regulated, WIF 1 were confirmed by real time PCR , while the gene HMGN1 had no confirmation of expression after real-time PCR. CONCLUSIONS: There is change in the gene expression of uterine leiomyoma of women undergoing treatment with GnRH analogue regarding women not treated. The number of genes underexpressed genes is double the down regulated and 80% of the changes detected by microarray were confirmed by real time PCR.
APA, Harvard, Vancouver, ISO, and other styles
3

Chen, Inne Lian, and 陳瑩蓮. "The regulation of gonadotropin-releasing hormone release by paminergic system in teleost." Thesis, 1993. http://ndltd.ncl.edu.tw/handle/01614996739145780649.

Full text
Abstract:
碩士
國立中山大學
海洋生物研究所
81
Dopamine has a inhibitory effect on the secretion of GTH. However, it is not clear whether the inhibtory effect of dopamine is directory acting on the gonadotroph or indirectly through the GnRH system. The purpose of this study is to set up a radioimmunoassay (RIA) to determine the concentration of salmon GnRH and to study the regulatory function of dopaminergic system on in vitro GnRH release. The synthetic salmon GnRH (sGnRH) was conjugated to bovine serum albumin (BSA) using bis-diazotized benidine (BDB) as a bridge and the sGnRH-BDB-BSA complex was used as a immunogen tonduce antibody for the RIA. Anti-sGnRH serum at the titer of 1:120,000 had a cross-reactivity with mammalian GnRH and chickennRH-I of 60.68% and 144.12% respectively, but had no significantross-reactivity with other peptides (TRH, Isotocin,g-vasotocin, Somatostatin). The replacement curve of sGnRHparallelism to mGnRH and cGnRH-I. Twenty-eight sex quiescenttilapia (Gonadosomatic index=0.125 ±0.06%) were sacrificede in vitro study of GnRH secretion. GnRH release from the-anterior hypothalamus (P-AH) and pituitaries in responsedopamine (2 hr), 10.8 uM pimozide (1 hr) and 60 mM K+ (1monitored at 15 minutes intervals. The results indicateddtable GnRH is released in vitro from both P-AH regionries in tilapia. However, there are no significantean concentration in response to dopamine orexperiment suggests that the dopaminergic systemant inhibitory function on GnRH secretion of malequiescent.
APA, Harvard, Vancouver, ISO, and other styles
4

HUANG, JIAN-SHUO, and 黃建碩. "Effects of aging and gonadal steroids on the release of gonadotropin releasing-hormone (GnRH) and luteinizing hormone (LH)." Thesis, 1989. http://ndltd.ncl.edu.tw/handle/51472703000778510203.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

塚原, 伸治, and Shinji Tsukahara. "The hypothalamic mechanisms controlling gonadotropin-releasing hormone release in rats : Pulse-generating and estrogen feedback mechanisms." Thesis, 1999. http://hdl.handle.net/2237/15772.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

葉濬毅. "Effect of chronic corticotropin-releasing factor infusion on gonadotropin-releasing hormone and gonadotropin releasl in ovariectomized rats." Thesis, 1992. http://ndltd.ncl.edu.tw/handle/24035730746420140383.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Books on the topic "Gonadotropin release hormone"

1

Ghazi, Nooshin. Variations in AII release from the rat brain during the estrous cycle. 1994.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Gonadotropin release hormone"

1

Terakado, Kiyoshi. "Induction of Gamete Release by Gonadotropin-Releasing Hormone (GnRH) in Ciona intestinalis." In The Biology of Ascidians, 125–30. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-66982-1_20.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Veldhuis, Johannes D. "Nature of Altered Pulsatile Hormone Release and Neuroendocrine Network Signalling in Human Ageing: Clinical Studies of the Somatotropic, Gonadotropic, Corticotropic and Insulin Axes." In Mechanisms and Biological Significance of Pulsatile Hormone Secretion, 163–89. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470870796.ch10.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Fuenzalida, Lidia C., Kim L. Keen, and Ei Terasawa. "Colocalization of FM1-43, Bassoon and GnRH-1: Possible GnRH-1 Release from the Cell Body and Their Neuroprocesses." In BASIC/TRANSLATIONAL - Gonadotropin-Releasing Hormone, P2–270—P2–270. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p33.p2-270.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Ramaswamy, Suresh, Stephanie B. Seminara, and Tony M. Plant. "Evidence from Studies of the Male Rhesus Monkey (Macaca mulatta) for the View That the Action of Neurokinin B to Trigger GnRH Release Lies Upstream from the Kisspeptin Receptor." In BASIC/TRANSLATIONAL - Gonadotropin-Releasing Hormone, P2–261—P2–261. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p33.p2-261.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Reynard, John, Simon Brewster, and Suzanne Biers. "Infertility." In Oxford Handbook of Urology, 551–66. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199696130.003.0012.

Full text
Abstract:
Male reproductive physiology 552 Aetiology and evaluation of male infertility 554 Investigation of male infertility 556 Oligozoospermia and azoospermia 560 Varicocele 562 Treatment options for male infertility 564 The hypothalamus secretes luteinizing hormone-releasing hormone (LHRH), also known as gonadotrophin-releasing hormone (GnRH). This causes the pulsatile release of anterior pituitary gonadotrophins called follicle-stimulating hormone (FSH) and luteinizing hormone (LH), which act on the testis. FSH stimulates the seminiferous tubules to secrete inhibin and produce sperm; LH acts on Leydig cells to produce testosterone (...
APA, Harvard, Vancouver, ISO, and other styles
6

Ojeda, Sergio R., and William J. Kovacs. "Organization of the Endocrine System." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0004.

Full text
Abstract:
Multicellular organisms are endowed with coordinating systems that regulate and integrate the function of the different cells composing these organisms. Two main interacting systems perform this critical function: the nervous system and the endocrine system. The former employs electrochemical signals to convey regulatory inputs to peripheral organs and to receive information from them; the latter produces chemical agents that, in general, are transported systemically by the bloodstream to the target organs. The two systems are closely interconnected. The most conspicuous connection is that of the hypothalamus and the pituitary gland. Hypothalamic neurosecretory cells produce substances that are delivered to the portal blood vessels (see Chapter 5) and transported to the anterior pituitary (adenohypophysis), where they regulate the secretion of adenohypophyseal hormones. Other hypothalamic neurons send their axons to the posterior pituitary, from which they release their neurosecretory products directly into the bloodstream. The nervous system also innervates most, if not all, endocrine glands, including the gonads, the thyroid, and the adrenals. The nerves control not only blood flow but also the secretion of hormones. In turn, the endocrine system regulates the function of the nervous system. For example, gonadal and adrenocortical hormones act directly on the central nervous system to either inhibit or to stimulate the secretion of neuropeptides involved in the control of the pituitary-gonadal and pituitary-adrenal axes, respectively (i.e., gonadotrophin-releasing hormone [GnRH], also known as luteinizing hormone-releasing hormone [LHRH], and corticotropin-releasing hormone [CRH]; see Chapter 5). Although conventional definitions of the nervous and endocrine systems emphasize their differences, the two systems also display similarities. For instance, the nervous system produces not only substances that act across synapses, but it also releases signaling molecules that reach distant target cells via the bloodstream.
APA, Harvard, Vancouver, ISO, and other styles
7

Shacham, Sharon, Dagan Harris, Herzel Ben-Shlomo, Inbar Cohen, David Bonfil, Fiorenza Przedecki, Hadas Lewy, Israel E. Ashkenazi, Rony Seger, and Zvi Naor. "Mechanism of GnRH receptor signaling on gonadotropin release and gene expression in pituitary gonadotrophs." In Vitamins & Hormones, 63–90. Elsevier, 2001. http://dx.doi.org/10.1016/s0083-6729(01)63003-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

ACKLAND, JACQUELINE F., BRIGITTE G. MANN, and NEENA B. SCHWARTZ. "Release of Immunoreactive Inhibin from Perifused Rat Ovaries: Effects of Forskolin and Gonadotropins during the Estrous Cycle." In Recent Progress in Hormone Research, 531–37. Elsevier, 1993. http://dx.doi.org/10.1016/b978-0-12-571148-7.50030-0.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Gonadotropin release hormone"

1

Ohlsson, M., A. J. W. Hsueh, and T. Ny. "HORMONE REGULATION OF THE FIBRINOLYTIC SYSTEM IN THE OVARY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644389.

Full text
Abstract:
In the ovary, the release of oocytes from graafian follicles during hormone-induced ovulation has been found to be associated with substantial increases in follicular plasminogen activator (PA) activity. Most of the PA activity comes from the granulosa cells that have been shown to produce tPA, uPA as well as the type-1 PA-inhibitor,(PAI-1).We have studied the molecular mechanism of follicle stimulating hormone (FSH) and gonadotropin releasing hormone (GnRH) on the synthesis of tPA in primary cultures of rat granulosa cells. FSH and GnRH were both found to induce tPA in granulosa cells in a time and dose dependent manner. The effect of FSH and GnRH on the levels of tPA mRNA was also studied by northern and slot blot hybridizations. FSH and GnRH were both found to increase the level of tPA mRNA. The stimulation was up to 18 -fold compared to untreated cells.The induction of tPA mRNA by FSH and GnRH was additive and the time courses of the stimulation by the hormones differed, suggesting that different cellular mechanisms are involved. Consistent with the ability of FSH to activate the cAMP dependent protein kinase A pathway, the phosphodiesterase inhibitor 1-methyl-3-isobutylxanthine further enhanced the FSH induction of tPA mRNA.GnRH is known to activate the phospholipid-dependent protein kinase C pathway. Likewise the effect of GnRH can be mimicked by the kinase C activator, phorbol myristate acetate.It is concluded that FSH and GnRH regulates tPA production by differnt molecular mechanisms, and that the increase in tPA activity is mediated via an increase in the levels tPA mRNA. Since both gonadotropins and GnRH cause ovulation in hyposectomized animals, similar stimulatory actions of these hormones on the tPA activity suggest a correlative relationship between this enzyme and the ovulatory process.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Gonadotropin release hormone' for particular source types:
Journal articles
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography