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1
Sheward, William John. "Thyrotrophin releasing hormone, somatostatin and luteinizing hormone releasing hormone : aspects of their synthesis, release and actions". Thesis, University of Edinburgh, 1986. http://hdl.handle.net/1842/20183.
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2
Stevens, Jeffrey David. "LHRH fusion protein vaccines in beef heifers and bovine ectopic ovarian xenografting". Online access for everyone, 2004. http://www.dissertations.wsu.edu/Dissertations/Fall2004/J%5FStevens%5F092204.pdf.
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CASTEL, VINCENT. "Les analogues de la luteinizing hormone-releasing hormone en pathologie uterine". Angers, 1990. http://www.theses.fr/1990ANGE1046.
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4
Wang, Jian. "Action of luteinizing hormone-releasing hormone in rat ovarian cells : hormone production and signal transduction". Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/29313.
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The present study was conducted to investigate the hypothesis that membrane phosphoinositide breakdown may participate in the actions of luteinizing hormone-releasing
hormone (LHRH) on hormone production in the rat ovary.
In granulosa cells prelabeled with [³H]-arachidonic acid
or [³H]-inositol, treatment with LHRH increased the accumulation of radiolabeled inositol lipids, diacylglycerol and free arachidonic acid, but luteinizing hormone (LH) or cholera toxin did not exert the same effect. Activation of protein kinase C by the phorbol ester, 12-0-tetradecanoyl phorbol-13-acetate (TPA) had a stimulatory action on membrane phosphoinositide breakdown. In addition, TPA did not alter arachidonic acid release but potentiated the A23187 stimulated liberation of arachidonic acid.
Changes in the cytosolic free calcium ion concentrations,
[Ca²⁺]i, induced by LHRH were studied in individual cells using
fura-2 microspectrofluorimetry. The resting [Ca²⁺]i was 96.7 ±
2.9 nM (n= 115). The alterations in [Ca²⁺]i induced by LHRH
were transient and returned to resting levels within 84±3
second (n=64). A potent LHRH antagonist completely blocked the
effect of LHRH on [Ca²⁺]i. Some cells responded to LHRH alone,
whereas others responded to angiotensin II, suggesting that
there are different subpopulations of granulosa cells.
Sustained perifusion of LHRH resulted in a desensitization of
the [Ca²⁺]i response to LHRH but not to the calcium ionophore
A23187. LHRH treatment accelerated [Ca²⁺]i depletion in granulosa cells perifused with Ca²⁺ free medium, indicating
the involvement of intracellular Ca²⁺ pool(s) in [Ca²⁺]i
changes induced by LHRH.
The complex interactions between the signal transduction
pathways involved in the regulation of progesterone and
prostaglandin E₂ were also examined. LHRH increased basal
progesterone level (5 and 24h culture) and attenuated
progesterone production induced by follicle-stimulating hormone
(FSH) or cholera toxin (24h). On the other hand, both basal
and FSH or cholera toxin stimulated prostaglandin E₂ formation
were increased by LHRH (5 and 24h) . A23187, TPA and melittin
(an activator of phospholipase A₂) were used to examine the
roles of Ca²⁺, protein kinase C and free arachidonic acid, respectively, in LHRH action. Melittin stimulated basal progesterone and prostaglandin E₂ production, and enhanced the stimulation of prostaglandin E₂ by LHRH, A23187 and TPA, indicating that LHRH alters cyclooxygenase activity. A23187 or TPA attenuated the formation of progesterone induced by FSH or cholera toxin (5 and 24h). In contrast, A23187 and TPA augmented cholera toxin or FSH induced prostaglandin E₂ formation. The stimulatory effects of A23187 and TPA on prostaglandin E₂ were synergistic, whether or not FSH or cholera toxin was present during the incubation.
The role of arachidonic acid in the action of LHRH was further investigated. Arachidonic acid enhanced progesterone production in a dose dependent manner and potentiated TPA induced progesterone production. The stimulatory effect of arachidonic acid was blocked by nordihydroguaiaretic acid, whereas monohydroxyeicosatetraenoic acids and
hydroperoxyeicosatetraenoic acid mimicked the effect of
arachidonic acid, suggesting the involvement of lipoxygenase
metabolites in LHRH action. In addition, arachidonic acid
partially reversed the inhibitory action of LHRH and TPA on
FSH induced progesterone production. Although arachidonic
acid, TPA and LHRH stimulated progesterone production,
arachidonic acid only slightly elevated 20-alpha-hydroxy-
progesterone production as compared to that induced by LHRH and
TPA. These results suggest that arachidonic acid or its
metabolites have a stimulatory role in the action of LHRH on
the de novo synthesis of ovarian steroid hormones.
Collectively, these findings support the hypothesis that
the actions of LHRH or LHRH like peptides on ovarian hormone
production are mediated by multiple second messengers involving
Ca²⁺, protein kinase C and arachidonic acid metabolites.Medicine, Faculty of
Cellular and Physiological Sciences, Department of
Graduate
5
Kallmeier, Robert Charles. "Molecular studies of luteinizing hormone-releasing hormones in the brain of domestic fowl". Thesis, University of Reading, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.306719.
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6
顔秀慧 i S. W. Ngan. "Transcriptional regulation of the human gonadotropin releasing hormonereceptor gene". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31240847.
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Albertson, Asher J. "Extra-pituitary functions for GnRH". Laramie, Wyo. : University of Wyoming, 2007. http://proquest.umi.com/pqdweb?did=1313910061&sid=1&Fmt=2&clientId=18949&RQT=309&VName=PQD.
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Ngan, S. W. "Transcriptional regulation of the human gonadotropin releasing hormone receptor gene /". Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21687584.
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9
Von, Boetticher S. "Investigating the mechanism of transcriptional regulation of the gonadotropin-releasing hormone receptor (GnRHR) gene by dexamethasone". Thesis, Link to the online version, 2008. http://hdl.handle.net/10019/1796.
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10
Wibullaksanakul, Sunee. "Regulation of gonadotropin releasing hormone (GnRH) secretion : in-vitro studies in the male rat". Thesis, The University of Sydney, 1992. https://hdl.handle.net/2123/26487.
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The study described in this thesis was carried out between 1986—1990 while the author was a postgraduate candidate at The University of Sydney, and in receipt of a scholarship from the Australian International Development Assistance Bureau (AIDAB), Department of Foreign Affairs and Trade. The author would like to thank AIDAB for its financial support.
During this time, all experimental work and data analysis was carried out by the author, with excellent technical assistance from Mrs Jennifer Spaliviero and Miss Elsa Kidston. Experimental work involving animals was approved by the University of Sydney Animal Ethics Review Committee. Matters of design and interpretation were closely supervised by Associate Professor David J Handelsman, whose invaluable advice the author wishes to acknowledge.
This thesis has been arranged into six related chapters. The first section is a literature review. This section outlines the current state of knowledge concerning general~ aspects of gonadotropin—releasing hormone (GnRH) function, regulatory mechanisms of hypothalamic GnRH secretion, and the methodology suitable for investigation of the regulatory mechanisms of GnRH secretion from the medial basal hypothalamus (MBH) of adult male rats. Both systems are compared for features of methodological integrity, including stability of baseline GnRH release and technical limitations or artefacts. In the third part of this work, these in-vitro methods are applied to examine the effect of castration on GnRH secretion, the results of which are discussed in chapter three. The fourth section of this project concerns the effects of steroids, opioids and noradrenergic signals on GnRH secretion from MBH of adult male rats. In the fifth section of this project, the effect of experimental uremia as a model disease on GnRH secretion is addressed. The last chapter of this project is a summary and discussion. Since each chapter is discussed in detail, the final section is an overview of the content of previous chapters.
11
Rodriguez, Rafael Eduardo 1963. "Regulation of LH and GnRH secretion during prepubertal development in the bull calf". Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277009.
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A series of experiments were conducted to investigate the regulatory mechanisms governing the absence of and the initiation of pulsatile pituitary LH secretion during the infantile and prepubertal periods of development in the bull calf. In the first experiment, patterns of hypothalamic GnRH secretion into hypophyseal portal vessels were measured in sixteen Holstein bull calves at 2, 5, 8 and 12 weeks of age. The results of this study correlated the attainment of an hourly rate of pulsatile GnRH release to the onset of prepubertal LH secretion. In the second experiment, nine Holstein bull calves were infused with exogenous GnRH (200 ng) on an hourly basis from 1 to 6 weeks of age. From this experiment, we were able to demonstrate that an hourly rate of pulsatile GnRH release stimulates the age-associated changes in the hypothalamic-pituitary axis necessary for initiating pituitary LH secretion during the transition from the infantile to prepubertal period of development.
12
李繼仁 i Kai-yan Lee. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31214332.
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Lee, Kai-yan. "Regulation of gonadotropin-releasing hormone and gonadotropin in goldfish, carassius auratus /". Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18038165.
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Cheung, Wai-ting. "Role of gonadotropin-releasing hormone of metastatic potential of ovarian cancer cells". Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B41634184.
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15
Layas, Fatima M. "Cholinergic involvement in the mechanisms regulating luteinizing hormone releasing hormone secretion in the domestic fowl". Thesis, University of Reading, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.292213.
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Green, Heather Joy. "Effects of hormonal treatments, appraisal, and coping on cognitive and psychosocial functioning of men with non-localised prostate cancer /". St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16139.pdf.
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17
Chik, Chi-chung Stanley. "Characterization of two chicken gonadotropin releasing hormone-II genes in goldfish, Carassius Auratus : y Chik Chi Chung Stanley". Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2056630X.
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18
Hoo, L. C., i 何麗莊. "Transcriptional regulation of the human gonadotropin-releasing hormone(GnRH) II and GnRH receptor genes". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29297011.
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Ma, Chi-him Eddie. "Molecular studies of gonadotropin releasing hormone receptors and estrogen receptors in goldfish (Carassius auratus)". Click to view the E-thesis via HKUTO, 2000. http://sunzi.lib.hku.hk/hkuto/record/B4257531X.
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Chen, Hui, i 陳慧. "Seasonal cycle of gonadal steroidogenesis and the effects of luteinizing hormone and luteinizing hormone releasing hormone on thein vitro and in vivo steroidal secretions in monopterus albus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1989. http://hub.hku.hk/bib/B31208514.
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21
Binder, April Kay. "The role of ß-catenin in the gonadotrope transcriptional network interactions with SF1 and TCF /". Pullman, Wash. : Washington State University, 2009. http://www.dissertations.wsu.edu/Dissertations/Fall2009/a_binder_090309.pdf.
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馬智謙 i Chi-him Eddie Ma. "Molecular studies of gonadotropin releasing hormone receptors and estrogen receptors in goldfish (Carassius auratus)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B4257531X.
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Lee, King-yiu. "Molecular cloning and characterization of gonadotropin-releasing hormone receptors in the black seabream (Mylio macrocephalus)". Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22823876.
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24
曾美好 i May-ho Tsang. "Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) secretion and gene expression in a GnRH neuronal cell line". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1995. http://hub.hku.hk/bib/B31213698.
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25
Tsang, May-ho. "Dopaminergic regulation of gonadotropin-releasing hormone (GnRH) secretion and gene expression in a GnRH neuronal cell line /". Hong Kong : University of Hong Kong, 1995. http://sunzi.lib.hku.hk/hkuto/record.jsp?B17095219.
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Bracken, Cynthia J. "Factors controlling ovarian follicular growth in sows /". free to MU campus, to others for purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3115527.
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27
Girmus, Ronald Leslie. "Direct ovarian steroid regulation of pituitary luteinizing hormone secretion, stores and subunit mRNA". Diss., The University of Arizona, 1992. http://hdl.handle.net/10150/185816.
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The ovarian steroids, progesterone and estradiol, regulate luteinizing hormone synthesis and secretion during the estrous cycle of mature ewes. During the luteal phase of the cycle the ovarian steroids inhibit luteinizing hormone secretion. Luteinizing hormone is secreted from the pituitary when stimulated by the hypothalamic neuropeptide, gonadotropin-releasing hormone. Ovarian steroids can inhibit luteinizing hormone secretion indirectly, by decreasing the secretion of gonadotropin-releasing hormone or directly, by modulating the response of the pituitary to gonadotropin-releasing hormone. These studies have examined the direct control of pituitary luteinizing hormone secretion by using an in vivo model in which endogenous gonadotropin-releasing hormone (GnRH) release has been ablated and replaced with exogenous GnRH release at a constant frequency. Progesterone directly inhibited pituitary LH secretion in an estradiol-dependent manner and this may not require inhibition of pituitary LH synthesis. Progesterone inhibition of pituitary luteinizing hormone secretion is associated with enhanced progesterone binding by the pituitary.
28
Maze, Timothy D. "Development of the induced gonadotropin surge mechanism in the prepubertal heifer". Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2525.
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Thesis (Ph. D.)--West Virginia University, 2002.Title from document title page. Document formatted into pages; contains viii, 71 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references (p. 61-70).
29
Cheung, Wai-ting, i 張慧婷. "Role of gonadotropin-releasing hormone of metastatic potential of ovarian cancer cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B41634184.
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30
Fernandes, S. M. (Sandra Maria). "Transcriptional regulation of the gonadotropin-releasing hormone receptor (GnRHR) gene by glucocorticoids". Thesis, Stellenbosch : Stellenbosch University, 2007. http://hdl.handle.net/10019.1/19595.
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Thesis (MSc)--University of Stellenbosch, 2007.ENGLISH ABSTRACT: The gonadotropin-releasing hormone (GnRH) receptor is a G-protein-coupled receptor in the pituitary gonadotropes and is an important control point for reproduction. GnRH binds to the GnRH receptor (GnRHR) resulting in the synthesis and release of follicle stimulating hormone (FSH) and luteinizing hormone (LH). The sensitivity of the pituitary to GnRH can be directly correlated with GnRHR levels. The mouse GnRHR promoter contains three cis elements containing binding sites for steroidogenic factor-1 (SF-1), namely site 1 (-15/-7), site 2 (-244/- 236) and site 3 (-304/-296) as well as an activator protein-1 (AP-1)-like consensus sequence (TGAGTCA) at position –336/-330. While sites 1 and 2 and the AP-1 site have been previously shown to be involved in regulation of transcription of the mouse GnRHR (mGnRHR) promoter in some cell lines, the role of site 3 has not been previously investigated. This study investigated whether transcription of the mGnRHR gene is regulated by GnRH and glucocorticoids in the LβT2 gonadotrope pituitary cell line, and the role therein of site 3 and the AP-1 site and their cognate proteins, using a combination of in vitro protein- DNA binding studies and promoter-reporter assays. The role played by site 3 and the AP-1 site in basal transcription of the mGnRHR gene in LβT2 cells was the first area of investigation during this study. Luciferase reporter plasmids containing 600 bp of the mGnRHR promoter were used where the site 3 and AP-1 sites were either wild-type or mutated. Two constructs were prepared from the wild-type construct, i.e. wild type (LG), site 3 mutant (m3) and AP-1 mutant (mAP-1). Transfection of LG, m3 and mAP-1 plasmids into LβT2 cells was carried out to determine the effect of these mutations on the basal expression of the mGnRHR gene. Mutation of site 3 resulted in a 1.5 fold increase in the transcriptional activity of the mGnRHR promoter. This suggests that site 3 plays a role in the inhibition of basal transcriptional levels of the mGnRHR promoter in LβT2 cells. Mutation of the AP-1 site resulted in a 50% decrease in basal transcriptional levels of the mGnRHR promoter in LβT2 cells. This suggests that the AP-1 site is involved in positively mediating the basal transcriptional response of the GnRHR promoter in LβT2 cells. Experiments towards the understanding of the mechanism of the cis elements (site 3 and AP-1 site) on the mGnRHR promoter were carried out along with the role of protein kinase A (PKA) pathways, proteins involved and the effect of varying doses for varying times of GnRH, as well as the overexpression of PKA and the SF-1 protein. It was found that site 3 and the AP-1 site are not involved in the GnRH response. Results suggest that site 3 is partially involved in the PKA response in LβT2 cells. Site 3 can bind SF-1 protein as shown via competitive electrophoretic mobility shift assays (EMSA). When EMSA’s were performed on the AP-1 site the findings were that the c-Fos protein was not involved in the activation of the AP-1 site. A factor was found to bind to the AP-1 site, which did not require the intact AP-1 site, suggesting that it could be the c-Jun protein that binds to the AP-1 site under basal conditions. Another area that was investigated was whether the mGnRHR promoter can be regulated by dexamethasone (dex) either via the AP-1 site or site 3. A dose and time-dependent increase in promoter activity was observed with dex. This effect appears to require site 3 and the AP-1 site, as shown by the complete loss of response when these sites were individually mutated, consistent with a functional interaction between site 3 and the AP-1 site in LβT2 cells.
AFRIKAANSE OPSOMMING: Die gonadotropienvrystellings hormoon (GnRH) reseptor is ‘n G-proteïen-gekoppelde reseptor in die pituitêre gonadotrope en is ’n belangrike beheerpunt vir reproduksie. GnRH bind aan die GnRH reseptor (GnRHR) met die gevolg dat follikel stimulerende hormoon (FSH) en luteïeniserende (LH) gesintetiseer en vrygestel word. Die sensitiwiteit van die pituitêre klier vir GnRH kan direk met GnRHR vlakke gekorreleer word. Die muis GnRHR promotor bevat drie cis elemente met bindingssetels vir steroïedogeniese faktor 1 (SF1), naamlik setel 1 (-15/-7), setel 2 (-244/-236) en setel 3 (-304/-296) sowel as ’n aktiveerder proteïen 1 (AP-1) tipe konsensus sekwens (TGAGTCA) in posisie -336/-330. Terwyl setels 1 en 2 en die AP-1 setel voorheen getoon is om by die regulering van transkripsie van die muis GnRHR (mGnRHR) promotor in party sellyne betrokke te wees, is die rol van setel 3 nog nie vantevore bestudeer nie. In hierdie studie is ondersoek of die transkripsie van die mGnRHR geen deur GnRH en glukokortikoïede in die LβT2 gonadotroop pituitêre sellyn gereguleer word, en die rol van setel 3 en die AP-1 setel en hulle binders, deur gebruik te maak van in vitro proteïen-DNA bindings studies en promotor-verslaggewer essais. Die rol wat setel 3 en die AP-1 setel in basale transkripsie van die mGnRHR gene in LβT2 selle gespeel het, was die eerste onderwerp wat in hierdie studie bestudeer is. Lusiferase verslaggewer plasmiede wat die eerste 600 bp van die mGnRHR promotor bevat het en waarin setel 3 en die AP-1 setels óf wilde tipe óf gemuteer was, is gebruik. Two konstrukte is vanaf die wilde tipe konstruk berei, naamlik wilde tipe (LG), ’n setel 3 mutant (m3) en ’n AP-1 mutant (mAP-1). Transfeksie van LG, m3 en mAP-1 plasmiede in LβT2 selle is deurgevoer om te bepaal wat die effek van hierdie mutasies op die basale ekspressie van die mGnRHR gene was. Mutasie van setel 3 het ’n 1.5-voudige toename in die transkripsionele aktiwiteit van die mGnRHR promotor tot gevolg gehad. Dit suggereer dat setel 3 ’n rol in die inhibisie van die basale transkripsievlakke van die mGnRHR promotor in LβT2 selle speel. Mutasie van die AP-1 setel het tot ‘n 50% verlaging in basale transkripsievlakke van die mGnRHR promotor in LβT2 selle gelei. Dit suggereer dat die AP-1 setel betrokke is in die positiewe bemiddeling van die basale transkriptionele respons van die GnRHR promotor in LβT2 selle. Eksperimente wat gemik was om die meganisme van die cis-elemente (setel 3 en die AP-1 setel) op die mGnRHR promotor te verklaar, asook om die rol van proteïen kinase A (PKA) paaie, proteïene daarby betrokke en die effek van varieende dosisse vir verskillende tye van GnRH, sowel as die oorekspressie van PKA en die SF-1 proteïen, is deurgevoer. Dit is gevind dat setel 3 en die AP-1 setel nie betrokke by die GnRH respons is nie. Die resultate suggereer dat setel 3 gedeeltelik betrokke is by die PKA respons van LβT2 selle. Setel 3 kan SF-1 proteïen bind soos getoon deur kompeterence elektroforetiese mobiliteits verskuiwings essais (EMSA). As EMSA’s deurgevoer is op die AP-1 setel is bevind dat die c-Fos proteïen nie betrokke is in die aktivering van die AP-1 setel nie. ’n Faktor is gevind om aan die AP-1 setel te bind wat nie ’n intakte AP-1 setel vereis het nie, wat gesuggereer het dat dit die c-Jun proteïen kan wees wat aan die AP-1 setel onder basale omstandighede bind. ’n Ander area wat ondersoek is, is of die GnRHR promotor gereguleer kan word deur deksametasoon (dex) óf via die AP-1 setel óf via setel 3. ’n Dosis en tyds-afhanklike toename in promotor aktiwiteit is waargeneem met dex. ’n Vereiste vir hierdie effek blyk om die teenwoordigheid van setel 3 en die AP-1 setel te wees, soos aangetoon deur die totale verlies aan response as hierdie twee setels individueel gemuteer is, en wat weereens in ooreenstemming met die funksionele interaksie tussen setel 3 en die AP-1 setel in LβT2 selle is.
31
戚賜聰 i Chi-chung Stanley Chik. "Characterization of two chicken gonadotropin releasing hormone-II genes in goldfish, Carassius Auratus". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31220629.
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Hutson, Alison M. Dunham Rex A. "Evaluation of LHRHa implants and injections on the production of channel catfish (Ictalurus punctatus) female x blue catfish (Ictalurus furcatus) male fry". Auburn, Ala., 2006. http://repo.lib.auburn.edu/2006%20Summer/Theses/HUTSON_ALISON_44.pdf.
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Dyer, Cheryl J. "The leptin-NPY axis in sheep /". free to MU campus, to others for purchase, 1997. http://wwwlib.umi.com/cr/mo/fullcit?p9841280.
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34
Sadie, Hanél. "Transcriptional regulation of the mouse gonadotropin-releasing hormone receptor gene in pituitary gonadotrope cell lines". Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019.1/1495.
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Thesis (PhD (Biochemistry))--University of Stellenbosch, 2006.Gonadotropin-releasing hormone (GnRH), acting via its cognate receptor (GnRHR) is the primary regulator of mammalian reproductive function. Pituitary sensitivity to GnRH can be directly correlated with GnRHR levels on the surface of the pituitary gonadotrope cells, which can be regulated at transcriptional, post-transcriptional and post-translational levels. This study investigated mechanisms of transcriptional regulation of mouse GnRHR expression in two mouse gonadotrope cell lines, αT3-1 and LβT2, using a combination of endogenous mRNA expression studies, promoter-reporter studies, a two-hybrid protein-protein interaction assay, Western blotting, and in vitro protein-DNA binding studies. In the first part of the study, the role of two GnRHR promoter nuclear receptor binding sites (NRSs) and their cognate transcription factors in basal and Protein Kinase A (PKA)-stimulated regulation of GnRHR promoter activity was investigated in αT3-1 cells. The distal NRS was found to be crucial for basal promoter activity in these cells. While the NRSs were not required for the PKA response in these cells, results indicate a modulatory role for the transcription factors Steroidogenic Factor-1 (SF-1) and Nur77 via these promoter elements. The second part of the study focused on elucidating the mechanism of homologous regulation of GnRHR transcription in LβT2 cells, with a view to defining the respective roles of PKA and Protein Kinase C (PKC) in the transcriptional response to GnRH. In addition, the respective roles of the NRSs, the cyclic AMP response element (CRE) and the Activator Protein-1 (AP-1) promoter cis elements, together with their cognate transcription factors, in basal and GnRH-stimulated GnRHR promoter activity, were investigated. Homologous upregulation of transcription of the endogenous gene was confirmed, and was quantified by means of real-time RTPCR. The GnRH response of the endogenous gene and of the transfected promoter-reporter construct required PKA and PKC activity, and the GnRH response of the promoter-reporter construct was found to be dependent on a functional AP-1 site. Furthermore, GnRH treatment resulted in increased binding of phosphorylated cAMP-response element binding protein (phospho-CREB) and decreased expression and binding of SF-1 to their cognate cis elements in vitro, and stimulated a direct interaction between SF-1 and CREB, suggesting that these events are also required for the full transcriptional response to GnRH. This study is the first providing detail regarding the mechanism of transcriptional regulation of GnRHR expression in LβT2 cells by GnRH. Based on results from this study, a model has been proposed which outlines for the first time the kinase pathways, the promoter cis elements and the cognate transcription factors involved in homologous regulation of GnRHR transcription in the LβT2 cell line. As certain aspects of this model have been confirmed for the endogenous GnRHR gene, the model is likely to be physiologically relevant, and provides new ideas and hypotheses to be tested in future studies.
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Styger, Gustav. "The role of steroidogenic factor-1 (SF-1) in transcriptional regulation of the gonadotropin-releasing hormone (GnRH) receptor gene". Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52572.
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Thesis (MSc)--Stellenbosch University, 2001.ENGLISH ABSTRACT: The GnRH receptor is a G-protein-coupled receptor in pituitary gonadotrope cells. Binding of its ligand, GnRH, results in synthesis and release of gonadotropin hormones luteinizing hormone (LH) and follicle stimulating hormone (FSH). Steroidogenic factor 1 (SF-1), a transcription factor, binds to specific sites in the promoter region of gonadotropin genes, and thus regulates transcription of these genes. The promoter region of the GnRHreceptor gene contains two SF-1-like binding sites, one at -14 to -8 (site 1) and another at -247 to -239 (site 2), relative to the methionine start codon. The role played by these two SF-1-like sites in basal transcription of the mouse GnRH receptor (mGnRH-R) gene in a pituitary precursor gonadotrope cell line, aT3 cells, was the first area of investigation during this study. Luciferase reporter constructs containing 580 bp of mGnRH-R gene promoter were prepared, where SF-1-like sites were either wildtype or mutated. Four such constructs were made, i.e. wildtype (LG), site 1 mutant (LGM1), site 2 mutant (LGM2) and mutated site 1 plus site 2 (LGM1/2). These constructs were transfected into aT3 cells to determine the effect of mutations of sites 1 and/or 2 on the basal expression of the mGnRH-R gene. Mutation of either site 1 or site 2 had no effect on basal expression of the mGnRH-R gene. It was found that only upon simultaneous mutation of both sites 1 and 2, a 50% reduction in basal transcription took place. The implications of this is that SF-1 protein seems to only require one intact DNA-binding site, to mediate basal transcription of the mGnRH-R gene, suggesting that these two sites lie in close proximity during basal transcription. The effect of the protein kinase A (PKA) pathway on the endogenous mGnRH-R gene was also investigated by incubating non- , transfected aT3 cells with the PKA activators, forskolin and 8-Br-cAMP. Similar incubations were also performed on the wild type and mutated site 1 constructs transfected into pituitary gonadotrope aT3 cells. It was found that forskolin and 8-Br-cAMP were able to increase endogenous mGnRH-R mRNA levels in a concentration-dependent fashion, showing that endogenous GnRH receptor gene expression is stimulated via a protein kinase A pathway. Similar results were obtained with the wildtype promoter construct, showing that the protein kinase A pathway stimulates transcription of the promoter. This effect was only seen with wild type and not with the mutated site 1. These results are consistent with a role for a SF-1-like transcription factor in mediating the protein kinase A effect via binding to the site 1 at position -14 in the GnRH receptor gene. A separate investigation was performed to determine whether 25-hydroxycholesterol (25-0HC) is a ligand for SF-1, by incubating aT3 cells transfected with the various constructs with 25-0HC. Results show a dose-dependant response, with an increase in gene expression at 1 μM and a decrease at higher concentrations, for both mutant and wild type constructs. This suggests that, if SF-1 is indeed the protein binding to sites 1 and 2, then 25-0HC is not a ligand for SF-1 protein in aT3 cells and that the effect of 25-0HC on the mGnRH-R gene is not mediated via site 1. The results indicate that these decreases of expression at the higher concentrations may be due to cytotoxic effects. Towards the end of the study the laboratory obtained a luminoskan instrument with automatic dispensing features. Optimisation studies on the luciferase and β-Gal assays were performed on the luminoskan in a bid to decrease experimental error. It was found that automation of these assays resulted in a decrease in experimental error, showing that future researchers could benefit substantially from these optimisation studies.
AFRIKAANSE OPSOMMING: Die GnRH reseptor is 'n G proteïen-gekoppelde reseptor in pituitêre gonadotroopselle. Binding van die ligand, GnRH, lei tot die sintese en vrystelling van die gonadotropien hormone, luteïniserende hormoon (LH) en follikel stimulerende hormoon (FSH). Steroidogeniese faktor-t (SF-1) is 'n transkripsie faktor wat aan spesifieke areas in die promotergebied van die gonadotropien hormone bind, en dus transkripsie van hierdie gene reguleer. Die promotergebied van die GnRH reseptor geen bevat twee SF-1 bindings areas, een by -14 to -8 (area 1) asook by -247 to -239 (area 2), relatief to die metionien beginkodon. Die rol wat hierdie twee SF-1 areas speel in basale transkripsie van die muis GnRH reseptor (mGnRH-R) geen in 'n pituïtêre voorloper gonadotroop sellyn, aT3 selle, was die eerste gebied van ondersoek gedurende hierdie studie. Plasmiede bestaande uit die 580 basispaar mGnRH-R promoter verbind aan 'n lusiferase geen is vervaardig, waar SF-1-soortige areas enersyds onveranderd gelaat is, of gemuteer is. Vier sulke plasmiede is vervaardig, nl. onveranderd (LG), area 1 mutant (LGM1), area 2 mutant (LGM2) en gemuteerde area 1 plus area 2 (LGM1/2). Hierdie plasmiede is gebruik om aT3 selle te transfekteer om die effek van mutasies van areas 1 en/of 2 op die basale ekspressie van die mGnRH-R geen te ondersoek. Daar is gevind dat mutasies van areas 1 of 2 geen effek op basale ekspressie op die bogenoemde geen gehad het nie. Slegs tydens gelyktydige mutasie van areas 1 en 2 het 'n 50% vermindering in basale transkripsie plaasgevind. Die implikasies hiervan is dat die SF-1 proteïen blykbaar slegs een volledige DNA-bindingsarea benodig om basale transkripsie van die mGnRH-R geen te reguleer. Dit wil dus voorkom of hierdie twee areas baie na aan mekaar geposisioneer is tydens basale transkripsie. Die effek van die proteïen kinase A (PKA) roete op die natuurlike mGnRH-R geen is ook ondersoek tydens inkubasie van nie-getransfekteerde aT3 selle met die PKA akiveerders, forskolin en 8-Br-cAMP. Soortgelyke inkubasie is ook gedoen op die onveranderde en gemuteerde area 1 plasmiede wat in aT3 selle getransfekteer is. Daar is gevind dat forskolin en 8-Br-cAMP daarin geslaag het om die natuurlike mGnRH-R geen mRNA vlakke op 'n konsentrasie-afhanklike wyse te vermeerder. Hierdie resultaat dui daarop aan dat die natuurlike mGnRH-R geen se ekspressie gestimuleer kan word via 'n proteïen kinase A roete. Soortgelyke resultate is verkry met die onveranderde promoter plasmied en dit wys ook daarop dat proteïen kinase A transkripsie deur die promoter kan stimuleer. Hierdie effek was slegs aanwesig met die onveranderde en nie met die gemuteerde area 1 plasmied nie. Die resultate stem ooreen met 'n rol vir SF-1 transkripsie faktor in die regulering van proteren kinase A effek deur middel van binding aan die area 1 by posisie -14 in die GnRH-R geen. 'n Afsonderlike ondersoek is gedoen om vas te stel of 25-hidroksiecholesterol (25-0HC) 'n ligand vir SF-1 is deur getransfekteerde aT3 selle met 25-0HC te inkubeer. Resultate toon 'n dosis-afhanklike respons met 'n verhoging in geen ekspressie by 1 μM en 'n verlaging met hoër konsentrasies vir beide onveranderde en gemuteerde plasmiede. Dit impliseer dat, indien SF-1 wel die faktor is wat aan areas 1 en 2 bind, 25-0HC nie die ligand vir SF-1 proteren in aT3 selle is nie en dat die effek van 25-0HC op die mGnRH-R geen nie gereguleer word via area 1 nie. Die verlaging in ekspressie gevind by die hoër konsentrasies is dalk die gevolg van sitotoksiese effekte. Teen die einde van die studie het die laboratorium luminoskan toerusting met outomatiese pipettering verkry. Optimiseringstudies van die lusifirase en β-Galtoetse is met die luminoskan gedoen in 'n poging om eksperimentele foute te minimaliseer. Daar is gevind dat outomatisering van hierdie toetse wel gelei het tot 'n verlaging in eksperimentele foute. Toekomstige navorsers kan dus grootliks voordeel trek uit hierdie optimiseringstudies.
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Chairil, Redna Auroret. "The effect of chicken luteinizing-hormone releasing-hormone (LHRH) -I and -II on gonadotrophin secretion in domestic fowl". Thesis, University of Reading, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307005.
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Webber, Kate M. "THE ROLE OF LUTEINIZING HORMONE IN ALZHEIMER DISEASE". Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1164836822.
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Clarkson, Jenny, i n/a. "Activation of Gonadotropin-releasing hormone neurons by Kisspeptin in the mouse". University of Otago. Department of Physiology, 2008. http://adt.otago.ac.nz./public/adt-NZDU20081208.114143.
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The gonadotropin-releasing hormone (GnRH) neurons are the final output neurons of a complex neuronal network that controls fertility in all mammals. The GnRH neurons reside in a scattered continuum throughout the anterior hypothalamus. The majority of GnRH neurons project an axon to the median eminence where GnRH is secreted into the hypophyseal-pituitary portal vessels from whence it travels to the anterior pituitary gland. GnRH acts on the gonadotrophs of the anterior pituitary gland to cause the secretion of luteinising hormone (LH) and follicle stimulating hormone (FSH) into the peripheral circulation. LH and FSH act on the gonads to control gametogenesis and steroidogenesis. This thesis focuses on two unanswered questions in reproductive neurobiology that are fundamental to fertility 1) how the GnRH neurons become activated at puberty to produce patterned GnRH secretion and 2) the nature of the positive feedback mechanism that drives the preovulatory GnRH and LH surges.
Recently, a novel neuropeptide called kisspeptin and its G-protein coupled receptor GPR-54 were found to be essential for pubertal activation of GnRH neurons, with GPR-54 mutation or deletion resulting in failed puberty and infertility in humans and mice. In addition, kisspeptin administration potently stimulates GnRH neuron-mediated gonadotropin secretion and advances the onset of pubertal maturation suggesting an important role for kisspeptin in the activation and perhaps post-pubertal modulation of GnRH neurons.
In this thesis I have used immunocytochemical, whole animal manipulations and knockout mouse approaches to investigate the role of kisspeptin in both the activation of GnRH neurons at puberty and in the estrogen positive feedback mechanism in the mouse.
I have demonstrated that kisspeptin neurons are located principally in the rostral periventricular area of the third ventricle (RP3V) and the arcuate nucleus (ARN), which are both known to be important areas for the modulation of GnRH neuronal activity. Kisspeptin fibres are found in abundance throughout the hypothalamus, but of particular interest are the kisspeptin fibres found in close apposition with a subset of GnRH neurons in the rostral preoptic area (rPOA).
The kisspeptin neurons in the RP3V are sexually dimorphic with up to ten times more neurons in the female than the male. The number of kisspeptin neurons in the RP3V increases throughout pubertal development reaching adult levels at the time of puberty in both males and females. In concert with the increase in the number of kisspeptin neurons in the RP3V there is an increase in the percentage of GnRH neurons in the rPOA which exhibited a close apposition with a kisspeptin fibre indicating that kisspeptin neurons may target GnRH neurons to activate them at puberty. Additionally, I demonstrate that the increase in the number of neurons in the RP3V of the female mouse approaching puberty is driven by estrogen secreted from the ovary.
A significant number of kisspeptin neurons in the RP3V were shown to express tyrosine hydroxylase (TH). The number and percentage of kisspeptin cells colocalised with TH cells in the RP3V did not change throughout the estrous cycle. Some colocalisation of kisspeptin and TH was observed at terminal appositions with GnRH neurons in the rPOA, though the magnitude of colocalisation also did not change throughout the estrous cycle.
I demonstrate that RP3V kisspeptin neurons are a critical part of the estrogen positive feedback mechanism which drives the preovulatory GnRH and LH surges. Kisspeptin neurons in the RP3V express steroid receptors and are activated by estrogen positive feedback. Loss of kisspeptin-GPR-54 signalling prevents the GnRH neurons from being activated by estrogen positive feedback indicating that the RP3V kisspeptin neurons not only contribute to the estrogen positive feedback mechanism, but are a critical component of the mechanism.
The results of these studies demonstrate that kisspeptin is an integral component in both the activation of GnRH neurons at puberty and in the estrogen positive feedback mechanism which drives the preovulatory GnRH and LH surges. Therefore, kisspeptin plays an important role in the neuroendocrine control of reproduction in the mouse.
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Franco, Sharone Elizabeth. "A comparison of regulatory mechanisms of luteinizing hormone prolactin and growth hormone exocytosis in permeabilized primary pituitary cells (Part 1) ; The effect of divalent cations on luteinizing hormone and prolactin exocytosis in permeabilized primary pituitary cells (Part 2)". Master's thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/27117.
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Miles, Lauren E. C. "Mammalian cell growth and proliferation mediated by the gonadotropin-releasing hormone (GnRH) receptor : role of novel interacting protein partners". University of Western Australia. Centre for Medical Research, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0090.
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[Truncated abstract] It is becoming increasingly obvious that cell signalling pathways are more complicated than we originally perceived. Research is revealing that, not only is there a multitude of new proteins involved in signalling cascades, but also that previously identified proteins may have additional, alternate roles in intracellular trafficking. Gonadotropin-releasing hormone (GnRH) in conjunction with its receptor (GnRHR), the primary regulator of reproduction in all species, is no exception. In the past few years it has become readily accepted that the classic linear GnRHR-Gαq/11 signalling pathway is not universal and that this receptor is involved in a far greater range of cellular activities than was previously considered. In particular, it is widely accepted that continuous administration of GnRH analogs results in an inhibition of growth of a number of reproductive-derived tumours and that this may, in part, be mediated by direct activation of GnRHs expressed on these cells. However, it is not fully understood how the GnRHR mediates these growth effects or whether such effects are unique to reproductive-derived cancer cells. Research within this thesis aimed to determine how the presence or absence of this receptor in different cell types might affect the ability of GnRH to directly mediate growth effects. We demonstrate that continuous treatment with a GnRH agonist (GnRHA) induces an anti-proliferative effect in a gonadotropederived cell line (LβT2) and also in HEK293 cells stably expressing either the rat or human GnRHR. The anti-proliferative effect was time- and dose-dependent and was specifically mediated via the GnRHR, as co-treatment of the GnRHRexpressing cell lines with a GnRH antagonist blocked the growth suppressive effect induced by GnRHA treatment. Cell cycle analysis revealed that the GnRHA treated HEK/GnRHR cell lines induced an accumulation of cells in the G2/M phase while a G0/G1 arrest was observed in LβT2 cells. Previous identification by our group of a potential interaction between the GnRHR and the transcription factor E2F4, an integral cell cycle regulatory protein, prompted further investigation as to the nature of this interaction. Bioluminescence energy transfer (BRET) was utilised to demonstrate that the GnRHR also interacts with E2F5, another member of the E2F family of cell cycle proteins that shares a high level of homology to E2F4. In addition, it was determined that the interaction between human GnRHR and E2F4, detected using BRET, was influenced by cell density.
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李景耀 i King-yiu Lee. "Molecular cloning and characterization of gonadotropin-releasing hormone receptors in the black seabream (Mylio macrocephalus)". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31224635.
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Van, Biljon Wilma. "The mammalian type II gonadotropin-releasing hormone receptor : cloning, distribution and role in gonadotropin gene expression". Thesis, Stellenbosch : University of Stellenbosch, 2006. http://hdl.handle.net/10019.1/17333.
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Dissertation (PhD)--University of Stellenbosch, 2006.ENGLISH ABSTRACT: Gonadotropin-releasing hormone (GnRH) is well known as the central regulator of the reproductive system through its stimulation of gonadotropin synthesis and release from the pituitary via binding to its specific receptor, known as the gonadotropin-releasing hormone receptor type I (GnRHR-I). The gonadotropins, luteinising hormone (LH) and follicle-stimulating hormone (FSH), bind to receptors in the gonads, leading to effects on steroidogenesis and gametogenesis. The recent finding of a second form of the GnRH receptor, known as the type II GnRHR or GnRHR-II, in non-mammalian vertebrates triggered the interest into the possible existence and function of a GnRHR-II in humans. The current study addressed this issue by investigating the presence of transcripts for a GnRHR-II in various human tissues and cells. While it was demonstrated that antisense transcripts for this receptor, containing sequence of only two of the three coding exons, are ubiquitously and abundantly expressed in all tissues examined, potentially full-length (containing all three exons), sense transcripts for a GnRHR-II were detected only in human ejaculate. Further analysis revealed that the subset of cells in the ejaculate expressing these transcripts is mature sperm. These findings, together with the reported role for GnRH in spermatogenesis and reproduction led to the further analysis of the presence of a local GnRH/GnRHR network in human and vervet monkey ejaculate or sperm. Indeed, such a network seems to be present in humans since transcripts for both forms of GnRH present in mammals, as well as transcripts for the GnRHR-I, are expressed in human ejaculate. Furthermore, transcripts for the GnRHR-II are expressed in both human and vervet monkey ejaculate. Thus, it would appear that locally produced GnRH-1 and/or GnRH-2 in the human male reproductive tract might mediate their effects on fertility via a local GnRHR-I, and possibly via GnRHR-II. Remarkably, in the pituitary, LH and FSH are present in the same gonadotropes, yet they are differentially regulated by GnRH under various physiological conditions. While it is well established that post-transcriptional regulatory mechanisms occur, the contribution of transcriptional regulation to the differential expression of the LHβ- and FSHβ-subunit genes is unclear. In this study, the role of GnRH-1 and GnRH-2 via the GnRHR-I and the GnRHR-II in transcriptional regulation of mammalian LHβ- and FSHβ genes was determined in the LβT2 mouse pituitary gonadotrope cell-line. It is demonstrated for the first time that GnRH-1 may affect gonadotropin subunit gene expression via GnRHR-II in addition to GnRHR-I, and that GnRH-2 also has the ability to regulate gonadotropin subunit gene expression via both receptors. Similar to other reports, it is shown that the transcriptional response to GnRH-1 of LHβ and FSHβ is low (about 1.4-fold for bLHβLuc and 1.2-fold for oFSHβLuc). In addition, evidence is supplied for the first time that GnRH-2 transcriptional regulation of the gonadotropin β subunits is also low (about 1.5-fold for bLHβLuc and 1.1-fold for oFSHβLuc). It is demonstrated that GnRH-1 is a more potent stimulator of bLHβ promoter activity as compared to GnRH-2 via the GnRHR-I, yet both hormones result in a similar maximum induction of bLHβ. However, GnRH-2 is a more efficacious stimulator of bLHβ transcription via the GnRHR-II than GnRH-1. No discriminatory effect of GnRH-1 vs. GnRH-2 was observed for oFSHβ promoter activity via GnRHR-I or GnRHR-II. By comparison of the ratio of expression of transfected oFSHβ- and bLHβ promoterreporters via GnRH-1 with that of GnRH-2, it is shown that GnRH-2 is a selective regulator of FSHβ gene transcription. This discriminatory effect of GnRH-2 is specific for GnRHR-I, as it is not observed for GnRHR-II, where GnRH-1 results in a greater oFSHβ- to-bLHβ ratio. These opposite selectivities for GnRHR-I and GnRHR-II on the ratios of oFSHβ:bLHβ promoter activity for GnRH-1 vs. GnRH-2 suggest a mechanism for fine control of gonadotropin regulation in the pituitary by variation of relative GnRHR-I vs. GnRHR-II levels. In addition, a concentration-dependent modulatory role for PACAP on GnRH-1- and GnRH-2-mediated regulation of bLHβ promoter activity, via both GnRHR-I and GnRHR-II, and of oFSHβ promoter activity, via GnRHR-I, is indicated. The concentration-dependent effects suggest the involvement of two different signalling pathways for the PACAP response. Together these findings suggest that transcription of the gonadotropin genes in vivo is under extensive hormonal control that can be finetuned in response to varying physiological conditions, which include changing levels of GnRH-1, GnRH-2, GnRHR-I and GnRHR-II as well as PACAP.
AFRIKAANSE OPSOMMING: Gonadotropien-vrystellingshormoon (GnRH) is bekend as die sentrale reguleerder van die voorplantingsisteem deur die stimulasie van gonadotropiensintese en - vrystelling vanaf die pituïtêre klier via binding aan ‘n spesifieke reseptor, die sogenaamde tipe I gonadotropien-vrystellingshormoonreseptor (GnRHR-I). Die gonadotropiene, lutineringshormoon (LH) en follikel-stimuleringshormoon (FSH), bind aan reseptore in die gonades waar dit steroïedogenese en gametogenese beïnvloed. Die onlangse ontdekking van ‘n tweede vorm van die GnRH-reseptor, bekend as die tipe II GnRHR of GnRHR-II, in nie-soogdier vertebrate het belangstelling in die moontlike bestaan en funksie van ‘n GnRHR-II in die mens gewek. Hierdie kwessie is aangeraak deur die teenwoordigheid van transkripte vir ‘n GnRHR-II in verskeie weefsel- en seltipes van die mens te ondersoek. Daar is aangetoon dat nie-sin transkripte vir hierdie reseptor, wat die DNA-opeenvolgings van slegs twee van die drie koderende eksons bevat het, oormatig uitgedruk word in al die weefseltipes wat ondersoek is. Daarteenoor is potensieel vollengte (bevattende al drie eksons) sin transkripte vir ‘n GnRHR-II in die mens slegs in semen gevind. Verdere analise het getoon dat dit volwasse sperma binne die semen is wat laasgenoemde transkripte uitdruk. Hierdie bevindinge, tesame met die aangetoonde rol vir GnRH in spermatogenese en reproduksie het gelei tot die verdere analise van die teenwoordigheid van ‘n lokale GnRH/GnRHR-netwerk in mens- en blouaapsemen of -sperm. So ‘n netwerk blyk om teenwoordig te wees in die mens, aangesien transkripte vir beide vorme van GnRH wat in soogdiere gevind word, asook transkripte vir die GnRHR-I, in menssemen uitgedruk word. Daarbenewens word transkripte vir die GnRHR-II uitgedruk in beide mens- en blouaapsemen. Dit wil dus voorkom asof lokaalgeproduseerde GnRH-1 en/of GnRH-2 in die manlike voortplantingstelsel van die mens hul effek op vrugbaarheid bemiddel via ‘n lokale GnRHR-I, en moontlik ook via GnRHR-II. Dit is opmerklik dat LH en FSH teenwoordig is in dieselfde gonadotroopselle van die pituïtêre klier en tog verskillend gereguleer word deur GnRH tydens verskeie fisiologiese kondisies. Terwyl dit bekend is dat post-transkripsionele reguleringsmeganismes teenwoordig is, is die bydrae van transkripsionele regulering tot die differensiële uitdrukking van die LHβ- en FSHβ-subeenheidgene minder duidelik. In hierdie studie is die rol van GnRH-1 en GnRH-2 via die GnRHR-I en die GnRHR-II in transkripsionele regulering van soogdier-LHβ- en -FSHβ-gene in die LβT2 muis pituïtêre gonadotroopsellyn bepaal. Dit is vir die eerste keer aangetoon dat GnRH-1 ‘n effek mag hê op gonadotropiensubeenheid-geenuitdrukking via GnRHR-II bykomend tot GnRHR-I, en dat GnRH-2 ook die vermoë besit om gonadotropiensubeenheid-geenuitdrukking via beide reseptore te reguleer. Soos deur ander studies aangetoon is die transkripsionele respons van LHβ en FSHβ tot GnRH-1 klein (ongeveer 1.4-voudig vir bLHβLuc en 1.2- voudig vir oFSHβLuc). Verder is daar vir die eerste keer bewys gelewer dat transkripsionele regulering van die gonadotropien β-subeenhede deur GnRH-2 ook gering is (ongeveer 1.5-voudig vir bLHβLuc en 1.1-voudig vir oFSHβLuc). Daar is aangetoon dat GnRH-1 ‘n sterker stimuleerder van bLHβ-promotoraktiwiteit is in vergelyking met GnRH-2 via die GnRHR-I, hoewel beide hormone tot ‘n soortgelyke maksimum induksie van bLHβ lei. GnRH-2 is egter ‘n meer effektiewe stimuleerder van bLHβ-transkripsie as GnRH-1 via die GnRHR-II. Geen verskille is gevind tussen die effekte van GnRH-1 en GnRH-2 op oFSHβ-promotoraktiwiteit via GnRHR-I of GnRHR-II nie. Wanneer die verhouding van uitdrukking van getransfekteerde oFSHβ- en bLHβ- promotor-verslaggewers via GnRH-1 met dié van GnRH-2 vergelyk is, is aangetoon dat GnRH-2 ‘n selektiewe reguleerder van FSHβ-geentranskripsie is. Hierdie diskriminasieeffek van GnRH-2 is spesifiek vir GnRHR-I aangesien dit nie vir GnRHR-II waargeneem word nie. GnRH-1 lei tot ‘n groter oFSHβ tot bLHβ-verhouding via GnRHR-II. Hierdie teenoorgestelde selektiwiteite van GnRHR-I en GnRHR-II op die verhoudings van oFSHβ tot bLHβ-promotoraktiwiteit vir GnRH-1 teenoor GnRH-2 suggereer dat daar ‘n meganisme bestaan vir die fyn regulering van gonadotropiene in die pituïtêre klier, deurdat die relatiewe vlakke van GnRHR-I teenoor GnRHR-II gevarieer word. Daarbenewens is ‘n konsentrasie-afhanklike moduleringsrol vir PACAP op GnRH-1- en GnRH-2-bemiddelde regulering van bLHβ-promotoraktiwiteit aangetoon, via beide GnRHR-I en GnRHR-II, asook op oFSHβ-promotoraktiwiteit via GnRHR-I. Hierdie konsentrasie-afhanklike effekte dui op die betrokkenheid van twee verskillende seinpadweë vir die PACAP-respons. Tesame suggereer hierdie bevindinge dat transkripsie van die gonadotropiengene in vivo onder ekstensiewe hormonale kontrole is wat verfyn kan word in respons to veranderlike fisiologiese kondisies. Laasgenoemde sluit veranderende vlakke van GnRH-1, GnRH-2, GnRHR-I en GnRHR-II asook PACAP in.
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Myers, Tanya R. "New techniques for the qualitative and quantitative measurement of naturally-occurring gonadotropin-releasing hormone analogues by mass spectrometry". unrestricted, 2007. http://etd.gsu.edu/theses/available/etd-04192007-112108/.
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Thesis (Ph. D.)--Georgia State University, 2007.Title from file title page. Gabor Patonay, committee chair; A.L. Baumstark, G. Davon Kennedy, Gregg Pratt, committee members. Electronic text (170 p. : ill. (some col.)) : digital, PDF file. Description based on contents viewed Dec. 10, 2007. Includes bibliographical references.
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Leitman, Nicole Renee. "Comparison of CIDR-based protocols to synchronize estrus in beef heifers". Diss., Columbia, Mo. : University of Missouri-Columbia, 2007. http://hdl.handle.net/10355/5085.
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Thesis (M.S.)--University of Missouri-Columbia, 2007.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file. Title from title screen of research.pdf file (viewed on March 31, 2008) Vita. Includes bibliographical references.
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Stansfield, S. C. "The contribution of the endogenous opioid peptides to the regulation of luteinizing hormone-releasing hormone secretion in the domestic fowl". Thesis, University of Reading, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.372668.
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Romano, Nicola, i n/a. "Rapid effects of estrogen on intracellular calcium levels in adult GnRH neurons". University of Otago. Department of Physiology, 2009. http://adt.otago.ac.nz./public/adt-NZDU20090310.144345.
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The gonadotropin-releasing hormone (GnRH) neurons of the hypothalamus are the principal regulators of reproductive function and are strongly modulated by estrogen (E₂). Several studies indicate that E₂ is able to influence GnRH neurons, both with "classical" long-term transcriptional effects, and with rapid non-transcriptional effects. One most interesting action of E₂ is that of modulating intracellular calcium concentration [Ca�⁺]I: this has been shown to happen in many different cell types, including embryonic models of GnRH neurons.
The aim of this project was to evaluate if these rapid effects of E₂ on [Ca�⁺]I also happen at the level of adult GnRH neurons. In order to study the acute effects of E₂ on calcium dynamics, a novel transgenic mouse line was generated, that allows real-time measurement of [Ca�⁺]I selectively in GnRH neurons in an acute brain slice preparation. Using this mouse line, our group has previously shown that these cells show spontaneous activity in the form of Ca�⁺ transients.
A first set of experiments was designed to define the effects of E₂ on spontaneous activity. E₂ was found to modulate [Ca�⁺]I in a activity-dependent manner: it increased the frequency of [Ca�⁺]I transients in about 50% of GnRH neurons with low spontaneous activity, whereas it decreased the frequency of the transients in more than 80% spontaneously active GnRH neurons. Different experiments were then performed in order to determine the molecular pathways that generates these opposite effects.
The inhibitory effect was reproduced by the membrane-impermeable compound E2-6-BSA, indicating that it happens through a membrane receptor. The E₂ isomer l7α-estradiol was also able to reproduce the inhibitory effect of E₂, suggesting the involvement of some non-classical receptor. This is also confirmed by the presence of this effect in estrogen-receptor β (ER-β) knock-out mice, which exclude the involvement of this receptor.
The stimulatory effect was found to be generated through a novel, indirect mechanism. It cannot be reproduced by E2-6-BSA nor by l7α-estradiol, and it is still present in the ER-β knock-out mice. The stimulation, though, can be reproduced in about 50% of cells with an ER-α selective agonist. As this receptor is not present in GnRH neurons, an indirect mechanism must be generating the stimulatory effect. Blockage of action potential mediated synaptic transmission with tetrodotoxin (TTX) did not block E₂ effects, but blockage of non-action potential mediated GABAergic transmission using the GABA[A] selective blocker gabazine completely abolished them. Our hypothesis is therefore that E₂ stimulates the generation of [Ca�⁺]I transients through estrogen-receptor a (ER-α) located in the terminals of GABAergic afferents. This modulation, in turn, is able to determine release of Ca�⁺ from IP₃-sensitive intracellular stores. To confirm this, we applied exogenous GABA to the neurons and found that it was able to initiate [Ca�⁺]I transients. Furthermore, removal of tonic GABAergic tone with gabazine was able to block spontaneous activity.
To further analyse the effects of E₂, Ca�⁺ imaging experiments were performed together with cell-attached patch clamp electrophysiological recordings in order to correlate the electrical activity with the calcium activity. Simultaneous recordings revealed a strong correlation between [Ca�⁺]I transients and bursts of action currents in adult GnRH neurons. E₂ was able to increase the electrical activity of GnRH neurons with low spontaneous activity, and inhibit that of highly active ones. Application of GABA to GnRH neurons resulted in increased firing, accompanied by an increase in [Ca�⁺]I.
These observations provide evidence for a complex mechanism of E₂ action on adult GnRH neurons, that may be important for the generation of the pulsatile release of this hormone.
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Hernandez, Jennifer A. "Efficiency of LHRH immunization as a male sterilization vaccine". Online access for everyone, 2004. http://www.dissertations.wsu.edu/Dissertations/Summer2004/J%5FHernandez%5F081204.pdf.
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White, Allison E. "Optimizing dose and mode of administration of luteinizing hormone releasing hormone analog for induced spawning of black sea bass, Centropristis striata /". Electronic version (Microsoft Word), 2004. http://dl.uncw.edu/etd/2004/whitea/allisonwhite.html.
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Leung, Kin-yue. "Involvement of NF-kB subunit p65 and retinoic acid receptors RARæ and RXRæ in the transcriptional regulation of the human GnRH II gene". Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B36367035.
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Lee, ChangWoo. "CIS- AND TRANS-ACTIVATION OF HORMONE RECEPTORS: THE LH RECEPTOR". Lexington, Ky. : [University of Kentucky Libraries], 2003. http://lib.uky.edu/ETD/ukybiol2003d00082/changwoo.pdf.
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Thesis (Ph. D.)--University of Kentucky, 2003.Title from document title page. Document formatted into pages; contains xix, 74p. : ill. Includes abstract. Includes bibliographical references (p. 62-72).