Дисертації з теми "Gonadotrophin Hormone Releasing Hormone (GnRH)"
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Dorling, A. A. V. "Sex steroid regulation of gonadotrophin-releasing hormone (GnRH) neurons." Thesis, University of Cambridge, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.598603.
Повний текст джерелаHoo, L. C., and 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.
Повний текст джерелаMeyer, Colette. "Characterisation of the direct antiproliferative effects of a gonadotrophin-releasing hormone analogue." Thesis, University of Edinburgh, 2012. http://hdl.handle.net/1842/6476.
Повний текст джерелаStavrou, Emmanouil. "Regulation of FOXO transcription factors by gonadotropin-releasing hormone." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5686.
Повний текст джерелаForsdike, Rachel Anne. "In utero development of sexually dimorphic gonadotrophin-releasing hormone (GnRH) secretion in sheep." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.620917.
Повний текст джерела曾美好 and 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.
Повний текст джерелаTsang, 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.
Повний текст джерелаWormald, Patricia J. "GnRH and neuropeptide regulation of gonadotropin secretion from cultured human pituitary cells." Doctoral thesis, University of Cape Town, 1988. http://hdl.handle.net/11427/27168.
Повний текст джерелаCorchuelo, Chavarro Sheryll Yohana [UNESP]. "GnRH/GnIH e seus receptores no sistema olfato-retinal de zebrafish." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/134047.
Повний текст джерелаFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
O hormônio liberador de gonadotropina (GnRH) é um dos fatores chaves na regulação neuroendócrina da reprodução dos vertebrados. Alguns peixes apresentam três variantes do GnRH: o GnRH1 envolvido na secreção de gonadotropinas, o GnRH2 que regula o comportamento alimentar e sexual e o GnRH3 expresso no bulbo olfatório e o nervo terminal cujas fibras nervosas inervam a retina e o epitélio olfatório. O zebrafish possui duas variantes do GnRH (GnRH2 e GnRH3), sendo o GnRH3 a variante hipofisiotrófica. Estudos mostram possível envolvimento do GnRH no sistema olfato-retinal. No sistema olfatório o GnRH regula a sensibilidade na detecção de alimento, o reconhecimento intra e interespecífico, entre outros. Na retina, o GnRH3 pode estar envolvido na acuidade visual e do processamento de informação da retina. Existem estudos que reportam a presença de receptores de GnRH em diferentes camadas da retina, no entanto ainda não é clara a presença de receptores no epitélio olfatório. Neste contexto, no presente estudo analisamos a localização do gnrh2, gnrh3 e seus receptores (gnrhr1,2,3 e 4) e do gnih (hormônio inibidor de gonadotropinas) no epitélio olfatório, a retina e o bulbo olfatório de machos e fêmeas adultos e comparamos a expressão destes genes em fêmeas em diferentes estágios de maturação gonadal. Para tanto, o RNA total do epitélio olfatório, retina, bulbo olfatório, cérebro e gônadas foi extraído. Com base na sequência dos genes gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3 e gnrhr4, primers forward e reverse foram desenhados para RT-PCR e qPCR. Sondas para a hibridização in situ também foram construídas para verificar os sítios de expressão destas moléculas no epitélio olfatório, retina e gônadas. Imunohistoquímica com os anticorpos anti-GnRH3 (BB8 e GF6) foram realizadas para localizar a proteína do GnRH3 nos tecidos analisados. O presente estudo apresenta um panorama da expressão do sistema...
The gonadotropin releasing hormone (GnRH) is one of the key factors involved in the neuroendocrine regulation of vertebrate reproduction. Some fish species have three GnRH variants: GnRH1 involved in gonadotropin secretion, GnRH2 regulating food and sexual behaviors and the GnRH3 which is expressed in the olfactory bulb and terminal nerve whose fibers innervate the retina and the olfactory epithelium. Two GnRH variants (GnRH2 and GnRH3) are present in the zebrafish, in which GnRH3 acts as the hypophisiotrophic variant. Recent studies have been showing the role of GnRH in the olfactory-retinal system. In the olfactory system, GnRH regulates food detection, and intra and interspecific recognition. In retina, GnRH3 may be involved in visual acuity modulation and retinal processing information. Moreover, studies have reported the presence of GnRH receptors in the retina, but not yet in the zebrafish olfactory epithelium. Therefore, the current study analyzed the presence of GnRH2, GnRH3 and its receptors (GnRH-R1,2,3 and 4) and GnIH (gonadotropin inhibitory hormone) in the olfactory epithelium, olfactory bulb, retina and in gonads of adult zebrafish. We also compared the expression of these genes during the different stages of ovarian maturation in zebrafish. For that, total RNA of the olfactory epithelium, olfactory bulb, retina and gonads was extracted with the PureLink® RNA Mini Kit(Ambion®). RT-PCR and qPCR analysis were performed using forward and reverse primers for gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3, gnrhr4 for . Probes for in situ hybridization were constructed to verify the expression sites of these molecules in the olfactory epithelium, retina, and gonads. Immunohistochemistry usinganti-GnRH3 antibodies (BB8 and GF6) were performed to identify the GnRH3 protein in these tissues. The current study presents a general expression view of GnRH/GnIH and their receptors in the olfactory epithelium-olfactory bulb-retinal axis during ...
FAPESP: 2014/02481-9
Corchuelo, Chavarro Sheryll Yohana. "GnRH/GnIH e seus receptores no sistema olfato-retinal de zebrafish /." Jaboticabal, 2015. http://hdl.handle.net/11449/134047.
Повний текст джерелаCoorientador: Rafael Henrique Nóbrega
Banca: Elisabeth Criscuolo Urbinati
Banca: Matias Pandolfi
Resumo: O hormônio liberador de gonadotropina (GnRH) é um dos fatores chaves na regulação neuroendócrina da reprodução dos vertebrados. Alguns peixes apresentam três variantes do GnRH: o GnRH1 envolvido na secreção de gonadotropinas, o GnRH2 que regula o comportamento alimentar e sexual e o GnRH3 expresso no bulbo olfatório e o nervo terminal cujas fibras nervosas inervam a retina e o epitélio olfatório. O zebrafish possui duas variantes do GnRH (GnRH2 e GnRH3), sendo o GnRH3 a variante hipofisiotrófica. Estudos mostram possível envolvimento do GnRH no sistema olfato-retinal. No sistema olfatório o GnRH regula a sensibilidade na detecção de alimento, o reconhecimento intra e interespecífico, entre outros. Na retina, o GnRH3 pode estar envolvido na acuidade visual e do processamento de informação da retina. Existem estudos que reportam a presença de receptores de GnRH em diferentes camadas da retina, no entanto ainda não é clara a presença de receptores no epitélio olfatório. Neste contexto, no presente estudo analisamos a localização do gnrh2, gnrh3 e seus receptores (gnrhr1,2,3 e 4) e do gnih (hormônio inibidor de gonadotropinas) no epitélio olfatório, a retina e o bulbo olfatório de machos e fêmeas adultos e comparamos a expressão destes genes em fêmeas em diferentes estágios de maturação gonadal. Para tanto, o RNA total do epitélio olfatório, retina, bulbo olfatório, cérebro e gônadas foi extraído. Com base na sequência dos genes gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3 e gnrhr4, primers forward e reverse foram desenhados para RT-PCR e qPCR. Sondas para a hibridização in situ também foram construídas para verificar os sítios de expressão destas moléculas no epitélio olfatório, retina e gônadas. Imunohistoquímica com os anticorpos anti-GnRH3 (BB8 e GF6) foram realizadas para localizar a proteína do GnRH3 nos tecidos analisados. O presente estudo apresenta um panorama da expressão do sistema...
Abstract: The gonadotropin releasing hormone (GnRH) is one of the key factors involved in the neuroendocrine regulation of vertebrate reproduction. Some fish species have three GnRH variants: GnRH1 involved in gonadotropin secretion, GnRH2 regulating food and sexual behaviors and the GnRH3 which is expressed in the olfactory bulb and terminal nerve whose fibers innervate the retina and the olfactory epithelium. Two GnRH variants (GnRH2 and GnRH3) are present in the zebrafish, in which GnRH3 acts as the hypophisiotrophic variant. Recent studies have been showing the role of GnRH in the olfactory-retinal system. In the olfactory system, GnRH regulates food detection, and intra and interspecific recognition. In retina, GnRH3 may be involved in visual acuity modulation and retinal processing information. Moreover, studies have reported the presence of GnRH receptors in the retina, but not yet in the zebrafish olfactory epithelium. Therefore, the current study analyzed the presence of GnRH2, GnRH3 and its receptors (GnRH-R1,2,3 and 4) and GnIH (gonadotropin inhibitory hormone) in the olfactory epithelium, olfactory bulb, retina and in gonads of adult zebrafish. We also compared the expression of these genes during the different stages of ovarian maturation in zebrafish. For that, total RNA of the olfactory epithelium, olfactory bulb, retina and gonads was extracted with the PureLink® RNA Mini Kit(Ambion®). RT-PCR and qPCR analysis were performed using forward and reverse primers for gnrh2, gnrh3, gnrhr1, gnrhr2, gnrhr3, gnrhr4 for . Probes for in situ hybridization were constructed to verify the expression sites of these molecules in the olfactory epithelium, retina, and gonads. Immunohistochemistry usinganti-GnRH3 antibodies (BB8 and GF6) were performed to identify the GnRH3 protein in these tissues. The current study presents a general expression view of GnRH/GnIH and their receptors in the olfactory epithelium-olfactory bulb-retinal axis during ...
Mestre
Constantin, Stéphanie. "Développement de la signalisation calcique dans les neurones à GnRH." Tours, 2004. http://www.theses.fr/2004TOUR4017.
Повний текст джерелаThe gonadotropin releasing hormone is essential to the reproduction. Secreted in a pulsatile manner, it controls the gonadotropic hormones secretion. GnRH neurons are in small number and are spread in the hypothalamic preoptic area. A migratory phase during the embryonic life, precedes the set up of the secretion. Mechanisms involved in the migratory state, as well as those involved in secretion, in particularly pulsatility, remain unknown. Using two models of nasal explants cultures, we studied modifications in calcium conductances during the in vitro development and factors potentially involved in neuronal synchronization. Our results have underlined a maturation in calcium conductances and their relative contribution in intracellular calcium signaling occurring during the in vitro development. They have also shown the existence of rhythmicity in electrical activity, and confirmed the role for GABA and GnRH, even if the involvement of others neurotransmitters cannot be eliminated
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.
Повний текст джерелаENGLISH 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.
Mirhadi, Eila. "Regulation of gonadotropin-releasing hormone (GnRH) transcript production in the goldfish ovary." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ38601.pdf.
Повний текст джерелаMiles, 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.
Повний текст джерелаMorton, Stephanie. "Effects of continuous treatment with gonadotropin-releasing hormone during the anovulatory season on gonadotropin secretion, follicular dynamics and ovulation in the mare." Texas A&M University, 2004. http://hdl.handle.net/1969.1/1551.
Повний текст джерелаNkwayana, Nonhlanhla. "β-arrestin interacting domains on the type II gonadotropin-releasing hormone (GnRH) receptor". Master's thesis, University of Cape Town, 2006. http://hdl.handle.net/11427/3178.
Повний текст джерелаIncludes bibliographical references.
Includes bibliographical references (leaves 74-81).
Over-expression of β-arrestin 1 in COS-l cells revealed that the mammalian type GnRH receptor can internalise in a β-arrestin dependent manner whereas the internalisation of the mammalian type I GnRH receptor is β-arrestin independent. investigate which domains on the mammalian type II GnRH receptor are required for β~arrestin dependent internalisation, chimeric receptors were created.
The mammalian type II GnRH receptor possesses an intracellular C-terminal tail that is known to play a role in desensitisation, internalisation and overall signalling in GPCRs. On the other hand, the mammalian type I GnRH receptor, which lacks a C-terminal tail, does not readily desensitise and undergoes slow internalisation compared to the mammalian type II GnRH receptor. Over-expression of ß-arrestin 1 in COS-l cells revealed that the mammalian type GnRH receptor can internalise in a ß-arrestin dependent manner whereas the internalisation of the mammalian type I GnRH receptor is ß-arrestin independent. investigate which domains on the mammalian type II GnRH receptor are required for ß-arrestin dependent internalisation, chimeric receptors were created. Firstly, a chimera in which the full length type II GnRH receptor C-terminal tail was added to the tail-less type I GnRH receptor (TI/T2tail) was created. This chimera internalised in a ß-arrestin and GRK dependent manner, demonstrating that the type II GnRH receptor C-terminal tail confers ß-arrestin JGRK dependent internalisation on the originally ß-arrestin/GRK insensitive GnRH receptor. Mutating the putative GRK and casein kinase phosphorylation sites (serines 338 and 339) on the C-terminal tail of TI/T2tail to alanine residues did not abolish ß-arrestin dependent internalisation but eliminated GRK dependent internalisation, suggesting that other regions on the C-terminal tail are required for ß-arrestin dependent internalisation. A second chimera, in which the whole third intracellular loop of the type II GnRH receptor was replaced with that of the type I GnRH receptor (T2/TIICL3), was created. This chimera could not utilise ß-arrestin in its internalisation, indicating that the third intracellular loop of the type II GnRH receptor is required for ß-arrestin dependent internalisation. An alignment of the amino acid sequences of the two mammalian GnRH receptor third intracellular loops identified a basic residue rich area (R234, R236 and K237) on the type II GnRH receptor that was absent on the type I GnRH receptor. Interestingly, the triple mutant (R234,236,K237 A) still internalised in a ß-arrestin dependent manner, however, truncation of the C-terminal tail of R234,236,K237A abolished the ability of the receptor to internalise in a ß-arrestin dependent manner. This result indicated that the C-terminal tail of the type II GnRH receptor was compensating for the absence of the three basic residues. To summarise, this thesis demonstrates that the C-terminal tail of the type II GnRH receptor can confer ß-arrestin dependent intemalisation on the type I GnRH receptor. Furthermore, the third intracellular loop, and more specifically, basic residues R234, R236 and K237 on the mammalian type II GnRH receptor are required for ß-arrestin dependent intemalisation.
Fletcher, Patrick Allen. "Modeling electrical spiking, bursting and calcium dynamics in gonadotropin releasing hormone (GnRH) secreting neurons." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2574.
Повний текст джерелаCline, Mark Andrew. "Efficacy of Synthetic Gonadotropin Releasing Hormone Analogs for Control of Ovulation During Estrus Synchronization Protocols." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/31372.
Повний текст джерелаMaster of Science
Nicola, Angela Cristina de [UNESP]. "Atividade dos neurônios noradrenérgicos do Locus coeruleus e o conteúdo de GnRH em ratas Wistar acíclicas." Universidade Estadual Paulista (UNESP), 2013. http://hdl.handle.net/11449/92094.
Повний текст джерелаFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Fundação para o Desenvolvimento da UNESP (FUNDUNESP)
As alterações nos componentes reprodutivos do eixo hipotálamo-hipófise-gônadas em muitas fêmeas de mamíferos determinam a transição gradual de ciclos reprodutivos regulares para ciclos irregulares, com perda de fertilidade. A interação dos neurônios do hormônio liberador de gonadotrofinas (GnRH) e esteróides gonadais representa função chave na neurobiologia do envelhecimento, pois a sobreposição temporal da senescência endócrina e neural está mecanicamente interligada pelas alças de retroalimentação. Estímulos do locus coeruleus (LC) para a área pré-óptica (APO) e eminência mediana são essenciais para a liberação das gonadotrofinas e seus neurônios apresentam receptores para estrógeno e progesterona, sugerindo controle dos esteróides ovarianos. Neste estudo foi avaliado a atividade de células neuronais localizadas em áreas e núcleos envolvidos com o controle de ação dos neurônios GnRH de ratas Wistar no período de transição para a aciclicidade. Para este trabalho foram utilizadas fêmeas Wistar cíclicas (4 meses) e acíclicas (18-20 meses) submetidas à decapitação ou perfusão às 10, 14 e 18 h na fase do diestro. Após serem retirados, os cérebros dos animais decapitados foram congelados e armazenados para posterior determinação do conteúdo de GnRH hipotalâmico e do conteúdo de noradrenalina e dopamina na APO. Os cérebros perfundidos foram cortados seriadamente em secções coronais de 30 μm para a APO e o LC e...
Changes in reproductive components of the hypothalamic-pituitary-gonadal axis in many female mammals determine the gradual transition from regular reproductive cycles to irregular cycles, with loss of fertility. The interaction of neurons of gonadotropin-releasing hormone (GnRH) and gonadal steroids represents key role in the neurobiology of aging, because the temporal overlap of endocrine and neural senescence is mechanically interconnected by feedback loops. Stimulation of the locus coeruleus (LC) for the preoptic area (POA) and median eminence are essential for the release of gonadotropins and their neurons have receptors for estrogen and progesterone, suggesting control of ovarian steroids. Therefore, in this study we evaluated the activity of neuronal cells located in areas and nuclei involved in the control of action of GnRH neurons of female rats during the transition to acyclicity. For this study, we used cyclic female (4 months) and acyclic (18-20 months) rats underwent perfusion or decapitation at 10, 14 and 18 h of diestrus day. The brains from decapitated animals, after removed, were frozen and stored for subsequent determination of the hypothalamic GnRH content and the noradrenaline and dopamine content in the POA. The perfused brains were serially cut into coronal sections of 30 μm to POA and LC and subsequently submitted to immunohistochemical labeling for Fos (FRA) and FRA / TH, respectively. For quantitative analysis of the POA were considered plates containing AVPe being the counting of neurons FRA-ir performed from the insertion of the box with...
FAPESP: 12/14464-6
Nicola, Angela Cristina de. "Atividade dos neurônios noradrenérgicos do Locus coeruleus e o conteúdo de GnRH em ratas Wistar acíclicas /." Araçatuba, 2013. http://hdl.handle.net/11449/92094.
Повний текст джерелаCo-orientador: Janete Aparecida Anselmo-Franci
Banca: Maristela de Oliveira Poletini
Banca: Jacqueline Nelisis Zanoni
Resumo: As alterações nos componentes reprodutivos do eixo hipotálamo-hipófise-gônadas em muitas fêmeas de mamíferos determinam a transição gradual de ciclos reprodutivos regulares para ciclos irregulares, com perda de fertilidade. A interação dos neurônios do hormônio liberador de gonadotrofinas (GnRH) e esteróides gonadais representa função chave na neurobiologia do envelhecimento, pois a sobreposição temporal da senescência endócrina e neural está mecanicamente interligada pelas alças de retroalimentação. Estímulos do locus coeruleus (LC) para a área pré-óptica (APO) e eminência mediana são essenciais para a liberação das gonadotrofinas e seus neurônios apresentam receptores para estrógeno e progesterona, sugerindo controle dos esteróides ovarianos. Neste estudo foi avaliado a atividade de células neuronais localizadas em áreas e núcleos envolvidos com o controle de ação dos neurônios GnRH de ratas Wistar no período de transição para a aciclicidade. Para este trabalho foram utilizadas fêmeas Wistar cíclicas (4 meses) e acíclicas (18-20 meses) submetidas à decapitação ou perfusão às 10, 14 e 18 h na fase do diestro. Após serem retirados, os cérebros dos animais decapitados foram congelados e armazenados para posterior determinação do conteúdo de GnRH hipotalâmico e do conteúdo de noradrenalina e dopamina na APO. Os cérebros perfundidos foram cortados seriadamente em secções coronais de 30 μm para a APO e o LC e...
Abstract: Changes in reproductive components of the hypothalamic-pituitary-gonadal axis in many female mammals determine the gradual transition from regular reproductive cycles to irregular cycles, with loss of fertility. The interaction of neurons of gonadotropin-releasing hormone (GnRH) and gonadal steroids represents key role in the neurobiology of aging, because the temporal overlap of endocrine and neural senescence is mechanically interconnected by feedback loops. Stimulation of the locus coeruleus (LC) for the preoptic area (POA) and median eminence are essential for the release of gonadotropins and their neurons have receptors for estrogen and progesterone, suggesting control of ovarian steroids. Therefore, in this study we evaluated the activity of neuronal cells located in areas and nuclei involved in the control of action of GnRH neurons of female rats during the transition to acyclicity. For this study, we used cyclic female (4 months) and acyclic (18-20 months) rats underwent perfusion or decapitation at 10, 14 and 18 h of diestrus day. The brains from decapitated animals, after removed, were frozen and stored for subsequent determination of the hypothalamic GnRH content and the noradrenaline and dopamine content in the POA. The perfused brains were serially cut into coronal sections of 30 μm to POA and LC and subsequently submitted to immunohistochemical labeling for Fos (FRA) and FRA / TH, respectively. For quantitative analysis of the POA were considered plates containing AVPe being the counting of neurons FRA-ir performed from the insertion of the box with...
Mestre
Phillips, Pumza Samantha. "The role of Gai in the Gonadotropin-releasing hormone (GnRH) receptor inhibition of cell proliferation." Master's thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/11787.
Повний текст джерелаIncludes bibliographical references (leaves 72-78).
The activation of Gonadotropin-releasing hormone receptor (GnRHR) by the GnRH ligand has been shown to mediate antiproliferative effects in extra-pituitary cells and in reproductive cancer cell lines. The GnRHR couples to Gαq in pituitary gonadotropes. However, the GnRHR expressed in reproductive cancer cell lines is thought to couple to Gαi. Recent evidence also suggests that the antiproliferative effects may be mediated via Gαq in these cells. Therefore our study involved determining the role of Gαi in the antiproliferative effects mediated by the GnRHR. The results suggest that the Gαi pathway could play a role in mediating the antiproliferative effects of GnRH.
Hess, Milan B. "The Effects of Prostaglandin F2a, Oxytocin and Gonadotropin Releasing Hormone on Ejaculate Characteristics in the Dog." Thesis, Virginia Tech, 2002. http://hdl.handle.net/10919/31135.
Повний текст джерелаMaster of Science
Pheiffer, Carmen P. "The role of steroidogenic factor-1 (SF-1) in gonadotropin-releasing hormone (GnRH) receptor gene regulation." Master's thesis, University of Cape Town, 1998. http://hdl.handle.net/11427/26970.
Повний текст джерелаJunaidi, Aris. "Contraception in dogs using a slow release implant containing the gonadotropin releasing hormone (GnRH) agonist deslorelin." Thesis, Junaidi, Aris (1998) Contraception in dogs using a slow release implant containing the gonadotropin releasing hormone (GnRH) agonist deslorelin. PhD thesis, Murdoch University, 1998. https://researchrepository.murdoch.edu.au/id/eprint/51710/.
Повний текст джерелаHoricks, Florence. "INVESTIGATION OF POTENTIAL ACTION MECHANISMS OF GONADOTROPIN-RELEASING HORMONE ANALOGUES TO PREVENT OVARIAN DAMAGE DURING CHEMOTHERAPY." Doctoral thesis, Universite Libre de Bruxelles, 2017. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/256747.
Повний текст джерелаDoctorat en Sciences biomédicales et pharmaceutiques (Médecine)
info:eu-repo/semantics/nonPublished
Spiker, Carlie Rae. "Suppression of cyclicity and estrous behavior in mares through immunization against a recombinant gonadotropin-releasing hormone antigen." Thesis, Manhattan, Kan. : Kansas State University, 2009. http://hdl.handle.net/2097/1660.
Повний текст джерелаWhite, Colin D. "Dissection of GnRH receptor-G protein coupling." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3885.
Повний текст джерелаBanerjee, Sayanti P. "A Mathematical Model for the Transition in Firing Patterns Across Puberty of a Gonadotropin-Releasing Hormone Neuron." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1357249691.
Повний текст джерелаWaite, Kerry L. "Generation of a FHV-1 Viral Vaccine Against Gonadotropin Releasing Hormone for Immunocontraception of Felines." Thesis, Virginia Tech, 2006. http://hdl.handle.net/10919/34458.
Повний текст джерелаMaster of Science
Bo, Peng. "Gonadotropin-releasing hormone (GnRH) regulates trophoblast invasion and vascular mimicry : involvement of cell-cell adhesion and proteolysis dynamics." Thesis, University of British Columbia, 2014. http://hdl.handle.net/2429/47028.
Повний текст джерелаSmith, Caitlin. "The gonadotropin-releasing hormone (GnRH) system: a comparison between breeding and non-breeding naked mole rats (Heterocephalus glaber)." Master's thesis, University of Cape Town, 2010. http://hdl.handle.net/11427/6194.
Повний текст джерелаSantra, Sumana. "Studies On Cloning And Characterization Of GnRH Receptor From The Pituitary Of Bonnet Monkey (Macaca Radiata) And Functional Studies With The Antiserum To GnRH Receptor." Thesis, Indian Institute of Science, 2000. http://hdl.handle.net/2005/165.
Повний текст джерелаSadie, Hanel. "Interaction of SF-1 and Nur77 proteins from a gonadotrope cell line with the promoter of the GnRH receptor gene : implications for gene regulation." Thesis, Stellenbosch : Stellenbosch University, 2001. http://hdl.handle.net/10019.1/52307.
Повний текст джерелаENGLISH ABSTRACT: The regulation of gonadotropin releasing hormone (GnRH) receptor numbers in the pituitary is a crucial control point in reproduction. Pituitary sensitivity to GnRH can be directly correlated with GnRH receptor levels, which can be regulated at transcriptional and post-transcriptional level. The proximal promoter of the mouse GnRH receptor gene contains two cis elements bearing the consensus sequence for a Steroidogenic Factor-l (SF -1) binding site. The distal site has previously been shown to be involved in basal and tissue-specific transcriptional regulation, whereas the function of the proximal site was not established. SF-I, a member of the nuclear receptor superfamily of transcription factors, is involved in the transcriptional regulation of a large number of genes involved in steroidogenesis and reproduction. The consensus SF-I binding site can serve as a binding site for several members of the nuclear receptor superfamily. The aim of this study was to investigate the binding of SF-I protein from the aT3-1 gonadotrope cell line to the two putative SF-I binding sites in the mouse GnRH receptor promoter in vitro, in order to provide supporting evidence for their functional roles in GnRH receptor gene regulation. It was shown by Western blotting that SF-I and Nur77, another nuclear receptor transcription factor, are both expressed in aT3-1 cells, in a manner that is influenced by cell culture conditions. Gel mobility shift assays using specific antibodies showed that both SF-I and Nur77 protein in aT3-1 nuclear extracts bind to both sites in a mutually exclusive fashion. As shown by competition assays using mutated versions of the two sites, Nur77 protein had different base pair requirements than that of SF-I protein for binding to the sites. Additionally, SF-I mRNA was shown by Northern blotting to be increased in aT3-1 cells in response to stimulation of the Protein Kinase A (PKA) pathway by forskolin. These results highlight unexpected degeneracy in so-called "consensus" nuclear receptor binding sites. Furthermore, since Nur77 protein is involved in the stress response of the hypothalamic-pituitary-adrenal (HPA) axis, the unexpected presence of Nur77 protein in a gonadotrope cell line has potentially important implications for cross-talk between the HPA and hypothalamic-pituitary-gonadal (HPG) axes.
AFRIKAANSE OPSOMMING: Daar bestaan 'n direkte verband tussen pituïtêre sensitiwiteit vir gonadotropien-vrystellingshormoon (GnRH) en GnRH-reseptorvlakke Die regulering van GnRH-reseptorvlakke op transkripsionele en post-transkripsionele vlak in die pituïtêre klier is belangrik by die beheer van voortplantingsfunksies. Die proksimale promotor van die GnRH-reseptorgeen in die muis bevat twee cis elemente met die konsensus volgorde vir 'n Steroidogenic Factor-l (SF-I) bindingsetel. Die distale element is betrokke by basale en weefsel-spesifieke transkripsionele regulering, maar die funksie van die proksimale element is nog nie vasgestel nie. SF-1 is 'n lid van die superfamilie van selkernreseptore en is betrokke by die transkripsionele regulering van gene verantwoordelik vir steroïedogenese en voortplanting. Die konsensus SF-I bindingsvolgorde kan dien as bindingsetel vir verskeie selkernreseptore. Ten einde 'n beter insig ten opsigte van die regulering van die GnRH reseptorgeen te verkry, is ondersoek ingestel na die binding van SF-I-proteïen, afkomstig van die aT3-1 pituïtêre gonadotroopsellyn, aan die twee moontlike SF-l bindingsetels in die GnRH-reseptor promotor, in vitro. Die Western-klad metode het getoon dat beide SF-l en Nur77, 'n ander selkernreseptor-transkripsiefaktor, in die aT3-1 sellyn uitgedruk word. Die uitdrukking is afhanklik van selkultuurtoestande. Elektroforetiese mobiliteitsessais met spesifieke antiliggame het getoon dat SF-l en Nur77 proteïene in aT3-1 selkernproteïenekstraksies eksklusief aan beide bindingsetels bind. Nur77 proteïen benodig ander basispare as SF-l proteïen om aan die bindingsetels te bind. Hierdie resultate dui op onverwagse degenerasie in sogenaamde "konsensus" selkernreseptor-bindingsvolgordes. Die Northern-kladmetode het ook getoon dat SF-l mRNA vlakke in aT3-1 selle styg wanneer die proteïenkinase A (PKA) pad gestimuleer word met forskolin. Aangesien Nur77 proteïen betrokke is by die stres-respons van die hipotalamus-pituïtêre klier-adrenale (HP A) aksis, hou die onverwagse teenwoordigheid van Nur77 proteïen in 'n gonadotroop-sellyn potensieel belangrike inplikasies in vir kommunikasie tussen die HPA-aksis en die hipotalamus-pituïtêre klier-gonadale (HPG) aksis.
Buttrey, Brad Sterling. "Human chorionic gonadotropin and gonadotropin-releasing hormone influence pregnancy survival and resynchronized ovulation before timed artificial insemination in Holstein cattle." Thesis, Manhattan, Kan. : Kansas State University, 2008. http://hdl.handle.net/2097/542.
Повний текст джерелаRoy, Deboleena. "The effects of melatonin and gonadal steroids on gonadotropin-releasing hormone (GnRH) regulation in hypothalamic GT1-7 neuronal cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ63732.pdf.
Повний текст джерелаDowd, Peter Dylan. "The photophysical characterisation of a fluorescence-based immunoassay for the detection of gonadotropin-releasing hormone, type-1 (GnRH-I)." Thesis, University of Strathclyde, 2013. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=24378.
Повний текст джерелаMorley, Michelle Gaye. "Cloning and characterisation of gonadotropin-releasing hormone (GnRH) receptors in the cichlid (Haplochromis burtoni) and the zebrafish (Danio rerio)." Master's thesis, University of Cape Town, 2003. http://hdl.handle.net/11427/6949.
Повний текст джерелаThe identification of multiple forms of gonadotropin-releasing hormone (GnRH) in a single species is becoming a common occurrence. The highly conserved chicken GnRH II is present along with one or two other GnRHs, composing a combination unique to particular species. This multifunctional peptide is widely distributed through the central nervous system and peripheral tissues. Also, endogenous GnRHs demonstrate distinct patterns of spatial expression within the brain, suggesting they may have separate functions. In addition to being the primary regulator of gonadotropin secretion in vertebrates, GnRH is also involved in the release of GH and prolactin and may fulfil a possible neuromodulatory role. GnRHs exert their actions through the stimulation of distinct GnRH receptors on pituitary gonadotrophs. The presence of multiple GnRH receptor subtypes has been demonstrated in several species and is likely to be a common characteristic of most vertebrates. This thesis describes the cloning and characterisation of GnRH receptors in two species of teleost fish, Haplochromis burtoni (cichlid) and Dania rerio (zebrafish). A type I GnRH receptor has previously been shown to exist in the cichlid. In the present study degenerate primers designed to extracellular loop three of the mammalian GnRH receptors were used to identify a second putative receptor subtype from cichlid (Haplochramis burtoni) genomic DNA. Furthermore, a near full-length cDNA, encompassing transmembrane domain 1 through to transmembrane domain 7 of the GnRH receptor, was cloned from cichlid RNA by reverse transcriptase PCR. This region of the receptor shares approximately 80% amino acid homology with corresponding regions of type III GnRH receptors previously identified in species of perciform fish. Partial sequences of a type IA and a type lB GnRH receptor have previously been identified in the zebrafish. Two sets of degenerate primers were used to elucidate the possible existence of a third receptor in the zebrafish using both genomic DNA and RNA. However, this strategy failed to result in the amplification of novel receptor subtypes in the zebrafish. Controversy surrounds the developmental origins of GnRH neurons and their temporal expression in relation to GnRH receptors. The zebrafish is a model organism, widely used for the study of reporter gene expression during development. Hence an attempt was made to isolate the zebrafish GnRH receptor genes using a genomic DNA library and identify the promoter regions for use as reporter genes in the study of GnRH and GnRH receptor expression during development. Southern blot analysis revealed six genomic clones with sequences homologous to zebrafish GnRH receptor cDNA. Comparison with genomic and cDNA sequences of other GnRH receptors revealed that those regions of the genomic clones that were sequenced only encoded exons 2 and 3. The presence of large introns in the GnRH receptor gene made it difficult to identify genomic clones containing the entire gene and the promoter region. The cloning of part of the zebrafish GnRH receptor genes will make their complete characterisation somewhat less problematic since an idea of their basic intron/exon structure has been obtained. Exons 2 and 3 of the zebrafish type IA and type IB GnRH receptor genes show a high degree of conservation when compared to the same regions of the goldfish type IA and type IB GnRH receptor cDNAs, demonstrating approximately 90% homology in both cases. In this study sequence information was obtained for the regions between transmembrane domains 4 and 7, and 3 and 7 of the zebrafish type IA and type IB GnRH receptor genes, respectively, and was subsequently used clone zebrafish GnRH receptor full-length cDNAs. This study describes the discovery of a type III GnRH receptor in the cichlid but suggests its presence may be restricted to only certain orders of teleost since a type III receptor was not identified in the zebrafish on this occasion. The information acquired from this study may help to reveal patterns, which relate the presence of particular GnRHs and GnRH receptors in single species to specific reproductive requirements.
Kinch, R. F. T. "Effects of age, photoperiod, and castration on the responsiveness of the pituitary gland of the vole, Microtus agrestis, to stimulation by gonadotrophin-releasing hormone (GnRH)." Thesis, Oxford Brookes University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374975.
Повний текст джерелаLiu, Tang-Yu. "A Mathematical Model for the Luteinizing Hormone Surge in the Menstrual Cycle." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1471606050.
Повний текст джерелаDeus, Daiane Beneduzzi de. "Estudo do gene do receptor de GnRH (GNRHR) no hipogonadismo hipogonadotrófico isolado normósmico e atraso constitucional do crescimento e desenvolvimento." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-02012014-165016/.
Повний текст джерелаGnRH receptor (GNRHR) inactivating mutations are the most common genetic cause of normosmic IHH. The genes involved in the IHH, including GNRHR, have been associated with a large phenotypic spectrum, varying from partial to complete IHH. Constitutional delay of growth and puberty (CDGP) might represent a mild phenotypic variant of IHH. In this study we investigated novel variants and characterized the frequency and phenotype-genotype correlation of GNRHR mutations in normosmic IHH and CDGP patients. Additionally, we determined de cause of the recurrence of GNRHR p.R139H mutation in patients with normosmic IHH. We studied 116 patients with normosmic IHH and 51 with CDGP. The control group was composed by 130 adults with normal pubertal development. The coding region of GNRHR was amplified and automatically sequenced. The two novel variants identified (p.Y283H, p.V134G) were submitted to in silico and in vitro analysis. Three microsatellite markers (D4S409, D4S2387, D4S3018) were amplified by PCR and analyzed in the patients with the p.R139H mutation. In the CDGP group, the previously described mutation p.Q106R was identified in the heterozygous state in one boy. The p.Q106R mutation has been identified in heterozygous state in individuals with normal pubertal development and does not appear be involved on the CDGP phenotype in this patient. In the normosmic IHH group, nine variants were identified (p.N10K, p.Q11K, p.Q106R, p.R139H, p.C200Y, p.R262Q, p.Y284C, p.Y283H, p.V134G) in eleven patients (9.5%). In vitro analysis of the novel variants p.Y283H and the p.V134G demonstrated that both of them cause complete loss of function of the receptor. The founder effect study revealed that all the p.R139H affected Brazilian patients presented the same haplotype, suggesting that the this mutation has a common ancestor in the Brazilian population. Nevertheless the affected Polish family presented a different haplotype, with only one marker in common with the Brazilian families and further studies would be necessary to determine the origin of the p.R139H mutation in the European population. In conclusion this study demonstrated that GNRHR was the most commonly affected gene in normosmic IHH, with a good genotype-phenotype correlation, and should be the first candidate gene for genetic screening in this condition. The results of the founder effect study suggested that the p.R139H mutation has a common ancestor in the Brazilian population. Finally, mutations in the GNRHR do not appear to be involved in the pathogenesis of CDGP
Tata, Brooke. "Evidence For the Requirement of the Vesicular Protein, Rabconnectin-3α, in the Activation and Maturation of the Gonadotropin-Releasing Hormone (GnRH) Neuronal Network". Sorbonne Paris Cité, 2015. http://www.theses.fr/2015USPCC132.
Повний текст джерелаGonadotropin-releasing hormone (GnRH) neurons are the master regulatory output of the hypothalamus-pituitary-gonadal axis for pubertal onset. Puberty is characterized by the maturation of neuronal circuits where synaptic inputs change in the regulation of GnRH neurons to achieve pubertal onset. The mechanisms underlying these modifications remain elusive, but could be linked to the maturation of GnRH neurons. Deviations in the regulation of GnRH neurodevelopment cause pubertal delay and fertility defects. We discovered a complex neurodevelopmental disorder in human patients with a mutation in DMXL2, which encodes a vesicular protein rabconnectin-3α (rbcn3-α). Rbcn3-α is a scaffolding protein important for neuron plasticity and neurotransmitter release and can be a link between neuron plasticity and neurodevelopmental disorders with pubertal defects. Conditional neuronal Dmx12 knock-out mice (Nes::Cre;Dmx12loxp/wt) exhibitpubertal deficits, infertility, and a loss of GnRH neurons. We found loss of neuronal Dmx12 impedes GnRH neuron maturation, where immature GnRH neurons are unable to respond to potent stimuli compounded with disruptions in the circadian timed LH surge. These data indicate immature GnRH morphologies disrupts the functioning of GnRH neuronal networks. Moreover, Nes::Cre;Dmx12loxp/wt mice have decreased hypothalamic VGluT2 and increased NMDAR1 mRNA. Cre-dependent viral filling of GnRH neurons in GnRH::Cre ' Dmx12wt/wt mice showed rbcn3-a-containing terminals contact GnRH dendritic spines associated with VgluT2 terminals, and in the GnRH soma. We demonstrate rbcn3-a as a key regulator of pubertal onset and the maturation and activation of GnRH neurons
Arruda, Jalsi Tacon. "Comparação entre dois protocolos para estimulação ovariana com agonista/antagonista do hormônio liberador de gonadotrofinas (GnRH) em mulheres submetidas ao primeiro ciclo de reprodução assistida." Universidade Federal de Goiás, 2013. http://repositorio.bc.ufg.br/tede/handle/tede/3814.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES
Infertility affects more couples and assisted reproduction techniques offer a possibility of treatment and the chance of having a child. Thus, the first attempt to ovulation induction is critical to the success of the cycle or even for future attempts is successful. Objective: To compare the protocols using GnRH agonist or antagonist for ovarian stimulation in normo-responders undergoing the first cycle of IVF/ICSI. Methods: we conducted a literature review on the history of ovulation induction controlled by medications. From the data available in the database of electronic medical records SISFERT used in the Laboratory of Human Reproduction (LabRep-HC-FM-UFG) a comparative retrospective observational study was conducted with 50 patients divided into two groups according to protocol: GnRH-agonist (leuprolide acetate 1 mg/day short protocol) or GnRHantagonist (Cetrorelix 0.25 mg/day), which received 150 IU/day of rFSH (follitropin alpha) and 250 µg of rhCG (alpha-coriogonadotrofina) in both groups. Results: Statistically significant differences were observed in the days of stimulation with rFSH, total dose of gonadotropin, days of use of GnRH, GnRH dose and total number of follicles (≥ 16 mm) on the day of the group rhCG GnRH agonist. There was no significant difference in other parameters, however, the number of oocytes retrieved was slightly higher in the GnRH agonist, but fertilization rate was higher in the GnRH-antagonist. Pregnancy rates and clinical chemistry were similar in both groups. Conclusions: although no significant differences in the results analyzed, the use of flexible antagonist protocol facilitates the handling and enables the patient using much lower doses of gonadotropins itself as the antagonist, reducing the cost of treatment when compared to the protocol with GnRH agonist.
A infertilidade afeta cada vez mais casais e as técnicas de reprodução assistida oferecem uma possibilidade de tratamento e a chance de ter um filho. Assim, a primeira tentativa de indução da ovulação é fundamental para o sucesso do ciclo ou, até mesmo, para que tentativas futuras sejam bem sucedidas. Objetivo: comparar os protocolos utilizando agonista ou antagonista do GnRH para estimulação ovariana em pacientes normo-respondedoras submetidas ao primeiro ciclo de FIV/ICSI. Métodos: foi realizada uma revisão da literatura sobre a história da indução da ovulação controlada por medicamentos. A partir dos dados disponíveis no banco de prontuários eletrônicos SISFERT utilizado pelo Laboratório de Reprodução Humana (LabRep–HC–FM–UFG), um estudo observacional retrospectivo comparativo foi conduzido com 50 pacientes distribuídas em dois grupos de acordo com o protocolo: GnRH-agonista (acetato de leuprolide 1 mg/dia protocolo curto) ou GnRH-antagonista (cetrorelix 0,25 mg/dia); e que receberam 150 UI/dia de rFSH (alfa-folitropina) e 250 µg de rhCG (alfa-coriogonadotrofina) em ambos os grupos. Resultados: foram observadas diferenças estatisticamente significativas nos dias de estimulação com rFSH, dose total de gonadotrofina, dias de uso do GnRH, dose total de GnRH e o número de folículos (≥ 16 mm) no dia do rhCG no grupo GnRH-agonista. Não houve diferença significativa nos outros parâmetros, no entanto, o número de oócitos recuperados foi ligeiramente maior no grupo GnRH-agonista, mas a taxa de fertilização foi maior no grupo GnRH-antagonista. As taxas de gravidez química e clínica foram similares nos dois grupos. Conclusões: embora não tenha havido diferenças significativas nos resultados analisados, o uso do protocolo flexível com antagonista facilita a manipulação pela paciente usuária e possibilita doses menores tanto de gonadotrofinas quanto do próprio antagonista, reduzindo o custo do tratamento quando comparado ao protocolo com agonista do GnRH
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.
Повний текст джерелаManetta, Luiz Alberto. "O efeito do sistema intra-uterino de levonorgestrel (SIU-LNG) no fluxo das artérias uterinas, volume uterino e espessura endometrial em pacientes com endometriose pélvica: estudo comparativo com o análogo de GNRH (GnRHa)." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/17/17145/tde-26092013-155810/.
Повний текст джерелаObjectives:The objective of the present study was to compare the uterine arteries pulsatility index (PI) and resistence index (IR), uterine volume and endometrial thickness changes promoted by the use of the levonorgestrel intrauterine device (LNG-IUD) and the gonadotropin-releasing hormone analogue (GnRHa)in patients with endometriosis. Methods: Seventy nine women aged 18 to 40 years were included in this randomized controlled trial. Eighteen was excluded based on the exclusion criteria. The patients were randomly allocated in two groups: 31 women who used the LNG-IUD (since one became pregnant before insertion and wasexcluded) and 30 who used monthly GnRHa injections. They were submitted to a transvaginal two dimensional ultrasound scan on the day the treatment started and 6 months later, for the evaluation of uterine arteries PI, uterine arteries RI, uterine volume and endometrial thickness. Results: The use of LNG-IUD promoted an ndometrial thickness decrease (6.08±3.00mm to 2.7±0.98mm; mean±SD) as does the use of GnRHa (6.96±3.82mm to 3.23±2.32mm). The uterine volume decreased in the GnRHa group (86.67±28.38cm3to 55.27±25.52cm3), but not in the LNG-IUD group (75.77±20.88cm3 to 75.97±26.62cm3). Uterine arteries PI increased in both groups : Uterine arteries PI: LNG-IUD right uterine arterie 2.38 ± 0.72 to 2.76 ± 0.99 and left uterine arterie 2.46 ± 0.70 to 2.87 ± 0.96, and GnRHa right uterine arterie 2.04 ± 0.59 to 3.12 ± 0.98 and left uterine arterie 2.24±0.59 to 3.15 ± 0.89. Uterine arteries RI increased in both arteries in GnRHa and only in the left uterine arterie in the LNG-IUD :Uterine arteries RI : LNG-IUD right uterine arterie 0.85 ± 0..08 to 0.88 ± 0.07 and left uterine arterie 0.86 ± 0.07 to 0.89 ± 0.06, and GnRHa right uterine arterie 0.81 ± 0.07 to 0.93 ± 0.09 and left uterine arterie 0.84 ± 0.06 to 0.93 ± 0.09 . However, the increase was significant higher in the GnRHa group. Conclusions: Both GnRHa and LNG-IUD promoted an endometrial thickness decrease and an increase in the uterine arteries PI. The uterine volume decreased in women who used GnRHa, but not in those who used LNG-IUD.
Schlick, Jean-Luc. "Etude des protéines antivirales de phytolacca americana (pokeweed) : mise en évidence d'un complexe protéique dans lequel l'activité de la PAP est inhibée ; réalisation de protéines chimériques associant la gonadotropin-releasing hormone (GnRH) à la PAP." Besançon, 2000. http://www.theses.fr/2000BESA2029.
Повний текст джерелаFernandes, 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.
Повний текст джерелаENGLISH 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.
Vanacker, Charlotte. "Etude du rôle de l’expression du récepteur Neuropiline-1 et de l’exocytose Calcium-dépendante dans le neurone à GnRH sur le développement et la maturation du système à GnRH et la physiologie de la reproduction." Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S038/document.
Повний текст джерелаFertility in mammals is the result of a long development and maturation process of the hypothalamic-pituitary-gonadal axis. The reproductive function is orchestrated by a small population of neurons, located in preoptic area of hypothalamus in rodents, and releasing in a pulsatile manner Gonadotropin-releasing hormon (GnRH) in the portal blood vessels, where it is transported to the anterior pituitary gland. GnRH neuropeptide triggers synthesis and release of the gonadotropins LH and FSH, which in turn stimulates development and function of the gonads. GnRH neurons differenciate extracerebraly in the nasal placode and migrate from the vomeronasal organ to the forebrain along olfactory/vomeronasal nerves. At birth, the system is ready, however it will undergo a maturation phase before reaching puberty, signing the beginning of fertility. Deficiency in GnRH release can lead to idiopathic hypogonadotropic hypogonadism (IHH), characterized by a defect in sexual maturation and delayed or no puberty, or even to Kallmann syndrome when the IHH is associated with a deficit in the sens of smell. These phenotypes could be linked to a defect during GnRH neuron migration period and a decrease of GnRH cells located in hypothalamus after birth. Numerous studies have described the influence of different molecules on the migration of GnRH neurons. Recently, the semaphorin family, well known for its chemotactic effects in some cell types, and particularly the semaphorin3A (Sema3A), has been described by our laboratory as an essential factor for the guidance of GnRH neurons during embryogenesis, and characterized as a « Kallmann gene ». However, the role of Sema3A, and its specific receptor Neuropilin-1 (Nrp1) in GnRH neurons remains to be elucidated. The first objective of my thesis was to determine the role of the expression of Nrp1 in GnRH neurons. The analysis of sexual maturation in mice in which Nrp1 expression was selectively knocked out in GnRH neurons revealed a precocious onset of puberty and overweight compared to control littermates, correlated with an accumulation of GnRH neurons in preoptic area. The study of the development of the GnRH system during embryogenesis has shown an increased number of cells during migration. In vivo and in vitro data suggested the involvement of Nrp1 signaling pathway in the survival of GnRH neurons, the control of their motility during migration, and their final positioning in the brain.The second objective of my thesis was to study the role of Calcium-dependent exocytosis, and thus neurosecretion, in GnRH neurons on their development. The monitoring of Gnrh::cre; iBot animals, in which calcium-dependent exocytosis is abolished by cleavage of VAMP2/synaptobrevin2 protein in GnRH neurons, showed the distinction of two different phenotypes. A subpopulation of mice underwent normal puberty onset, with a similar bodyweight than control littermates, and the other one never reached puberty and developed overweight. The later animals exihibited IHH, increase of the volume of perigonadic fat tissue, and hyperleptinemia, with no alteration of GnRH neuron number and distribution. This data established that neurosecretion in GnRH neurons is not a prerequisite for their migration during embryonic development but revealed that it could play an important role in metabolic homeostasis.Together these two studies highlight an intriguing direct connection between GnRH neurons and energy metabolism in mammals as well as new mechanisms that could be implicated in reproductive physiopathology in human
Armstrong, Stephen Paul. "Pulsatile Gonadotrophin-releasing Hormone Receptor Signalling." Thesis, University of Bristol, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.526055.
Повний текст джерелаBettles, Stephen Paul. "Advancement of ovulation in yellowtail flounder, Pleuronectes ferrugineus, using gonadotropic hormone-releasing hormone analogue (GnRHa)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23118.pdf.
Повний текст джерелаAlbertson, 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.
Повний текст джерела