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Ghuman, Sarvpreet Singh. "Neuroendocrinology of stress and reproduction interaction." Thesis, University of Liverpool, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403220.
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Claudiano, Gustavo da Silva [UNESP]. "Aspectos da fisiopatologia da sepse em Piaractus mesopotamicus induzida por Aeromonas hydrophila." Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/128025.
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000849627.pdf: 553636 bytes, checksum: 5dfc24590b221b9994b1d94923ed02d2 (MD5)A patogenia da sepse envolve múltiplas inter-relações na dinâmica entre os diversos componentes relacionados ao hospedeiro e ao patógeno, com altas taxas de mortalidade em várias espécies animais. Embora seja uma das principais causas de mortalidade de peixes, há escassez de literatura sobre seus fenômenos fisiopatológicos e em seus mecanismos de modulação. Assim, neste trabalho, objetivou-se estudar os aspectos fisiopatológicos da evolução da reposta séptica induzida por Aeromonas hydrophila em Piaractus mesopotamicus - pacus. O inóculo utilizada foi determinada pela DL50 (DL50-96h) e estimada em 1,78 x 109. A sepse foi induzida pela inoculação na cavidade celomática e seguiram-se as coletas de sangue nos tempos pré-determinados de 1, 3, 6 e 9 horas após indução e o grupo controle. Verificou-se rápido aumento da cortisolemia com inibição da absorção de glicose, seguido de hipocortisolemia e hiperglicemia. Os hormônios da tireoide, apresentando diminuição imediata de suas concentrações séricas T3 e T4. Este último apresentou aumento 6 HPI. As alterações hormonais induzidas pela sepse desencadearam alterações nas vias metabólicas com aumento do catabolismo protéico e lipídico, utilização da via da glicólise anaeróbica transitória e lesão hepática. O leucograma demonstrou leucopenia e trombocitopenia seguido de cessar da quimiotaxia dos leucócitos após 6 HPI e graves alterações morfológicas em leucócitos e eritrócitos. As variáveis do sistema imune inato apresentaram aumento da produção de EROs 3 HPI, seguido de diminuição, sem alteração da concentração da lisozima sérica e progressivo aumento do ALS e AAB. Após inoculação ip. de A. hydrophila, foram evidenciados sinais clínicos de aeromonose, bacteremia crescente e sobrevida de 57,14 % depois 36 HPI
The pathogenesis of sepsis involves multiple interrelationships in the dynamics between various components related to the host and the pathogen, with high mortality rates in several animal species. Although it is a major cause of fish deaths, there is lack of literature about its physiopathology and the mechanisms of modulation. This work aimed to study the physiopathological aspects of the evolution of the septic response induced by Aeromonas hydrophila in Piaractus mesopotamicus - pacu. The dose was determined by the LD50 (LD50-96h) and estimated in 1,78 x 109. Sepsis was induced by the administration in the coelomic cavity and was followed by the collection of blood in the pre-determined times of 1, 3, 6, and 9 hours after induction and more control. There was a rapid increase of cortisol concentration in plasma, inhibition of glucose uptake, followed by hypocortisolemia and hyperglycemia. Thyroid hormones have immediate reduction of serum concentration of T3 and T4. The latter showed an increase after 6 HPI. Hormonal changes induced by sepsis-triggered changes in metabolic pathways enhancing protein and lipid catabolism, use of transient anaerobic glycolysis via and liver damage. The leucocyte count showed leukopenia and thrombopenia followed by cessation of leukocyte migration after 6 HPI and severe morphological changes in leukocytes and erythrocytes. The innate immune variables showed increased production of ROS after 3 HPI, followed by reduction without changing the concentration of serum lysozyme and progressive increase in SHA and ABA. After ip inoculation of A. hydrophila in pacu, clinical signs were evident of Aeromonas infection, growing bacteremia and survival of 57,14 % after 36 HPI
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Claudiano, Gustavo da Silva. "Aspectos da fisiopatologia da sepse em Piaractus mesopotamicus induzida por Aeromonas hydrophila /." Jaboticabal, 2015. http://hdl.handle.net/11449/128025.
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Orientador: Flávio Ruas de MoraesCoorientador: Julieta Rodini Egracia de Moraes
Coorientador: Cleni Mara Marzocchi-Machado
Banca: Aureo Evangelista Santana
Banca: Rogério Salvador
Banca: Luiz Lehmann Coutinho
Banca: Antonio Vicente Mundim
Resumo: A patogenia da sepse envolve múltiplas inter-relações na dinâmica entre os diversos componentes relacionados ao hospedeiro e ao patógeno, com altas taxas de mortalidade em várias espécies animais. Embora seja uma das principais causas de mortalidade de peixes, há escassez de literatura sobre seus fenômenos fisiopatológicos e em seus mecanismos de modulação. Assim, neste trabalho, objetivou-se estudar os aspectos fisiopatológicos da evolução da reposta séptica induzida por Aeromonas hydrophila em Piaractus mesopotamicus - pacus. O inóculo utilizada foi determinada pela DL50 (DL50-96h) e estimada em 1,78 x 109. A sepse foi induzida pela inoculação na cavidade celomática e seguiram-se as coletas de sangue nos tempos pré-determinados de 1, 3, 6 e 9 horas após indução e o grupo controle. Verificou-se rápido aumento da cortisolemia com inibição da absorção de glicose, seguido de hipocortisolemia e hiperglicemia. Os hormônios da tireoide, apresentando diminuição imediata de suas concentrações séricas T3 e T4. Este último apresentou aumento 6 HPI. As alterações hormonais induzidas pela sepse desencadearam alterações nas vias metabólicas com aumento do catabolismo protéico e lipídico, utilização da via da glicólise anaeróbica transitória e lesão hepática. O leucograma demonstrou leucopenia e trombocitopenia seguido de cessar da quimiotaxia dos leucócitos após 6 HPI e graves alterações morfológicas em leucócitos e eritrócitos. As variáveis do sistema imune inato apresentaram aumento da produção de EROs 3 HPI, seguido de diminuição, sem alteração da concentração da lisozima sérica e progressivo aumento do ALS e AAB. Após inoculação ip. de A. hydrophila, foram evidenciados sinais clínicos de aeromonose, bacteremia crescente e sobrevida de 57,14 % depois 36 HPI
Abstract: The pathogenesis of sepsis involves multiple interrelationships in the dynamics between various components related to the host and the pathogen, with high mortality rates in several animal species. Although it is a major cause of fish deaths, there is lack of literature about its physiopathology and the mechanisms of modulation. This work aimed to study the physiopathological aspects of the evolution of the septic response induced by Aeromonas hydrophila in Piaractus mesopotamicus - pacu. The dose was determined by the LD50 (LD50-96h) and estimated in 1,78 x 109. Sepsis was induced by the administration in the coelomic cavity and was followed by the collection of blood in the pre-determined times of 1, 3, 6, and 9 hours after induction and more control. There was a rapid increase of cortisol concentration in plasma, inhibition of glucose uptake, followed by hypocortisolemia and hyperglycemia. Thyroid hormones have immediate reduction of serum concentration of T3 and T4. The latter showed an increase after 6 HPI. Hormonal changes induced by sepsis-triggered changes in metabolic pathways enhancing protein and lipid catabolism, use of transient anaerobic glycolysis via and liver damage. The leucocyte count showed leukopenia and thrombopenia followed by cessation of leukocyte migration after 6 HPI and severe morphological changes in leukocytes and erythrocytes. The innate immune variables showed increased production of ROS after 3 HPI, followed by reduction without changing the concentration of serum lysozyme and progressive increase in SHA and ABA. After ip inoculation of A. hydrophila in pacu, clinical signs were evident of Aeromonas infection, growing bacteremia and survival of 57,14 % after 36 HPI
Doutor
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Honaramooz, Ali. "Neuroendocrinology of gonadotrophin secretion in prepubertal heifers." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ37889.pdf.
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Burmeister, Sabrina Suzanne. "Behavioral neuroendocrinology of the green treefrog (Hyla cinerea) /." Full text (PDF) from UMI/Dissertation Abstracts International, 2001. http://wwwlib.umi.com/cr/utexas/fullcit?p3008291.
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Gutzler, Stephanie. "The Neuroendocrinology of Seasonal Aggression in Female Syrian Hamsters." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/biology_diss/61.
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Aggression is a feature of many clinical disorders including autism, Alzheimer’s disease, bipolar disorder, and schizophrenia. The available treatment options act to prevent impulsive aggression through modulation of GABAergic and dopaminergic pathways which come with metabolic and dyskinetic side effects. The mechanism underlying aggressive motivation, however, has not been elucidated. In addition, previous studies have been heavily biased towards males of various species. Mimicking changes in day length, or photoperiod, in the laboratory is a natural manipulation used to examine seasonal changes in aggressive behavior in many species. In response to the reduction in the duration of light exposure, animals undergo gonadal regression and become reproductively quiescent. During this non-breeding season in male photoperiod-responsive animals, aggressive behavior increases significantly. Although studies have shown offensive aggression remains elevated in female rodents, seasonal regulation of this behavior in females has not been thoroughly studied. The neuropeptide arginine-vasopressin (AVP) has been implicated in the facilitation of aggressive behavior in male rodents and fishes; therefore, it is useful to examine AVP as a modulator of seasonal aggression in females. Because the actions of AVP in female social behavior may be hormonally-dependent, we investigated the hormonal mechanisms that regulate the expression of AVP receptors and the behavioral actions of AVP on aggression. In addition to changes in gonadal steroid hormones during the non-breeding season, we identified photoperiod-dependent alterations in adrenal hormone secretion as AVP plays a role in regulation of hypothalamic-pituitary-adrenal axis (HPA) activity and anxiety-like behaviors in animal models.
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Sunnasy, Dharmadeho. "Stress related changes in urinary biogenic amines in humans." Thesis, University of Greenwich, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307885.
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Herbison, Allan E. "The medical preoptic gaba system and its role in regulating luteinising hormone secretion." Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.385415.
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Bornstein, Stefan R. "From Neuroendocrinology to Neuroimmunomodulation – A Tribute to Prof. Dr. Samuel McCann." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135755.
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One of the leading experts in the field of Neuroendocrinology and Neuroimmunmodulation, Samuel Mac Donald McCann, known by all his friends as ‘Don’, passed away in 2007. This article pays tribute to his outstanding scientific contribution and a glimpse on his fascinating personality. A member of the National Academy of Sciences of the United States and pioneer in the field of neuroendocrine regulation, he identified numerous hormones and peptides and set the stage for basic concepts in physiology and clinical medicineDieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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McCann, John Patrick. "Pulmonary neuroendocrinology in health and disease : an immunocytochemical and radioimmunoassay study." Thesis, Queen's University Belfast, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259343.
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Bornstein, Stefan R. "From Neuroendocrinology to Neuroimmunomodulation – A Tribute to Prof. Dr. Samuel McCann." Karger, 2007. https://tud.qucosa.de/id/qucosa%3A27673.
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One of the leading experts in the field of Neuroendocrinology and Neuroimmunmodulation, Samuel Mac Donald McCann, known by all his friends as ‘Don’, passed away in 2007. This article pays tribute to his outstanding scientific contribution and a glimpse on his fascinating personality. A member of the National Academy of Sciences of the United States and pioneer in the field of neuroendocrine regulation, he identified numerous hormones and peptides and set the stage for basic concepts in physiology and clinical medicine.Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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Ferreira, Regis Cavini. "Respostas autonômicas e neuroendócrinas à recuperação de memórias traumáticas." Universidade de São Paulo, 2006. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-17082006-144725/.
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Diversos procedimentos são capazes de induzir a recuperação de memórias traumáticas (RecMem). Técnicas de psicoterapia têm sido usadas para reduzir a resposta emocional às memórias traumáticas, através de processos de re-estruturação e re-significação das vivências, baseados na resiliência dos sujeitos. Durante a RecMem podem ocorrer sinais clínicos de ativação autonômica que não são reações devidas a estressores externos. Pelo contrário, constituem o resultado de estímulos de natureza psíquica gerados internamente. Assim, é possível se especular se eles podem funcionar como estressores puramente psicológicos e, como tais, induzir respostas autonômicas e neuroendócrinas. O objetivo deste trabalho é o de se determinar se estas respostas ocorrem, assim como o de identificar suas características qualitativas e quantitativas. Seis voluntários de ambos os sexos, previamente selecionados e avaliados por testes psicológicos (SICD, Hamilton e BDI) e de cronotipagem, foram submetidos a duas condições: 1. condição controle (CC), e 2. condição de recuperação (CR). Em ambas as condições, os sujeitos foram colocados em ambiente controlado, com coleta de material destinado a dosagens de ACTH, adrenalina, cortisol, prolactina, TSH e GH (hormônios envolvidos com as respostas ao estresse), a cada 15 minutos, por 2 horas, com a primeira coleta 30 minutos antes do início dos procedimentos. Em ambas as condições, os sujeitos repousaram durante estes 30 minutos. Na CC os sujeitos permaneceram em repouso e na CR foram submetidos aos processos de RecMem, com seguimento psicoterapêutico subseqüente. Os dados obtidos foram avaliados quanto ao perfil das curvas tempo e resposta para cada hormônio e submetidos a testes estatísticos de comparação da secreção hormonal em ambas as condições. Concluímos que existiram respostas autonômicas e neuroendócrinas compatíveis com estresse psicológico que não são constantes em todos os sujeitos, onde se ressalta a variabilidade das respostas individuais obtidas.Several procedures are capable to induce retrieval of traumatic memories (RecMem). Psychotherapy techniques have been used to reduce the traumatic memories emotional response through rebuilding and re-meaning of the traumatic memories based on the subject´s resilience. Clinical signs of autonomic activation may be seen during RecMem, not representing reactions to external stressors. On the contrary, they are the result of psychic inputs internally generated. Therefore, it is possible to speculate that they can act as pure psychological stressors and, as such, able to induce autonomic and neuroendocrine responses. The aim of the present report is to determine whether these responses actually happen, as well as to determine their qualitative and quantitative characteristics. Six volunteers of both sexes, previously selected, and submitted to psychological testing (SCID, Hamilton and BDI) as well as chronotype determination, were submitted to two conditions: 1. Control condition (CC) and 2. Retrieval condition (CR). The subjects were placed in a controlled environment in both conditions, with ACTH, cortisol, adrenalin, prolactin, TSH and GH (stress related hormones) blood testing at every 15 minutes, for 2 hours; the first sample was obtained 30 minutes before the beginning of the procedures. In both conditions the subjects rested during these 30 minutes. In the CC the subjects remained resting, and in the CR were submitted to RecMem procedures followed by psychotherapeutic support. The resulting data were analyzed in their time-response curve profiles as well as were submitted to hormonal secretion statistical evaluation in both conditions. We conclude for autonomic and neuroendocrine responses compatible with psychological stress, that are not the same in all subjects, high lightening the variability of individual obtained responses.
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Sáenz, de Miera Cristina. "The role of photoperiodic history and internal long-term timing in seasonal neuroendocrinology." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=225273.
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Seasonal physiology has evolved as an adaptive strategy to changing environments with daylength (photoperiod) used as the predominant environmental cue to suit breeding and other functions to the external season. However, seasonal physiological state is determined not only by the photoperiod that is currently in effect but also by the animal's history, allowing changes in physiology in anticipation to the seasons. Many mammals and birds show internally timed, long-term (circannual) changes in seasonal physiology, synchronised to the seasons by changing photoperiods. The importance of history-dependent photoperiodic programming applies also to puberty attainment in juvenile animals, timed by the photoperiod received by the mother during gestation. In this project I investigated the effects of both types of history-dependent timing on the neuroendocrine pathways for photoperiodic regulation of seasonal physiology. In mammals, photoperiod is transmitted via the pineal hormone melatonin, which acts on the pars tuberalis (PT) to regulate thyrotropin (TSH) expression and in turn controls seasonal physiology via effects on the hypothalamic synthesis of type 2 and 3 thyroid hormone deiodinases (Dio2 and Dio3), and thus the local regulation of thyroid hormone metabolism, and downstream changes in hypothalamic neuropeptidergic signalling. Using two circannual species, the Soay sheep (Ovis aries) –a short-day breeder – and the European hamster (Cricetus cricetus) – a long-day breeder – exposed to constant photoperiodic conditions, my findings reveal that in both models, in the absence of seasonal cues, internal circannual timing is initiated at the PT control of TSH and transmitted to the regulation of hypothalamic T3 regulation and neuropeptides. Siberian hamsters (Phodopus sungorus) were placed under different photoperiods during gestation and transferred to a photoperiod of intermediate duration at weaning. Reproductive activation under these conditions was dependent upon early life exposure and this effect controls history-dependent changes in hypothalamic deiodinases. Interestingly, the gestational experience was reflected in PT TSH expression and Dio2 expression as early as birth time. The same prenatal effects were observed in a strain of seasonal mice, (Mus musculus molossinus). Overall my dissertation has established that: i) both the circannual and the melatonin signals converge on TSH expression to synchronise seasonal biological activity; ii) the photoperiodic pituitary-hypothalamic network is programmed by prenatal experience; and iii) this pathway is already functional before birth. Overall, my results highlight the PT as a conserved central site in mammals for the integration of multiple seasonal cues which via differential control of thyroid hormone levels in the hypothalamus dictates the timing in seasonal physiology.
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O'Brien, John Tiernan. "Magnetic resonance imaging and hypothalmic-pituitary-adrenal axis function in depression and Alzheimer's disease." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308774.
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Hassouna, Rim. "Rôles des peptides dérivés de la préproghréline dans le contrôle de la sécrétion de GH et du comportement alimentaire." Phd thesis, Université René Descartes - Paris V, 2012. http://tel.archives-ouvertes.fr/tel-00781915.
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Ghréline et obestatine sont deux hormones isolées à partir du tractus gastro-intestinal et issues du clivage protéolytique du même précurseur : la préproghréline. La ghréline est un peptide de 28 acides aminés qui subit une acylation sur sa sérine en position 3 lui permettant de se lier au récepteur des GH sécrétagogues (GHS-R). Ainsi la ghréline stimule la sécrétion de l'hormone de croissance (GH), hormone ayant également un rôle dans la modulation du métabolisme énergétique. En plus de son rôle en faveur de la sécrétion de GH, la ghréline est le seul peptide orexigène du tractus gastro-intestinal et un puissant facteur adipogène. L'obestatine isolée plus récemment à partir du tractus gastro-intestinal a été initialement décrite comme ayant un rôle anorexigène mais les données physiologiques concernant le rôle de ce peptide sont rapidement devenues contradictoires. Parallèlement, des données issues du laboratoire ont montré que l'obestatine avait une action antagoniste des effets de la ghréline exogène sur la sécrétion de GH et la prise alimentaire chez le rongeur mais que cette interaction n'avait pas lieu au niveau hypophysaire. Ainsi, nous avons émis l'hypothèse selon laquelle une interaction au niveau central entre la ghréline et l'obestatine est nécessaire au maintien de l'homéostasie des systèmes neuroendocrines contrôlant la croissance, la composition corporelle et la balance énergétique chez l'adulte. Dans un premier temps, il était nécessaire de déterminer le lieu de l'interaction entre ces deux peptides. Nous nous sommes donc intéressés aux neurones à NPY et GHRH du noyau arqué de l'hypothalamus (ArcN) qui expriment le GHS-R et sont la cible de la ghréline pour ses actions sur la prise alimentaire et la sécrétion de GH. Nos résultats montrent que l'obestatine et un variant naturel, l'obestatine Q90L, retrouvé parmi les patientes anorexiques à indice de masse corporelle (IMC) bas, ont un effet antagoniste sur la sécrétion de GH, la prise alimentaire et l'activité neuronale induites par la ghréline au niveau des neurones à NPY et GHRH de l'ArcN chez la souris. Une grande variabilité interindividuelle en réponse à la ghréline est observée et les effets antagonistes de l'obestatine ne sont visibles que chez les souris qui répondent bien à la ghréline, ce qui pourrait expliquer pourquoi les effets de l'obestatine ont été difficiles à caractériser jusqu'à présent.Afin de déterminer le rôle de la balance ghréline/obestatine dans le contrôle de la sécrétion de GH et la prise alimentaire, nous avons tiré parti de souris déficientes pour le gène de la préproghréline (ghrl-/-) qui n'expriment ni ghréline ni obestatine et chez lesquelles les deux peptides peuvent être remplacés pour en étudier l'impact. En effet, les ratios ghréline/obestatine sont modifiés dans plusieurs pathologies associées à des déséquilibres de la balance énergétique et de l'axe GH/IGF-1 mais l'impact physiologique de ces ratios déséquilibrés n'est pas connu. Nous avons, tout d'abord, caractérisé l'axe GH/IGF-1 ainsi que le comportement alimentaire chez les souris ghrl-/- et montré qu'elles n'avaient pas de phénotype permettant de les différencier des souris sauvages en ce qui concerne la taille, le poids ou encore le comportement alimentaire. Ces données sont en accord avec d'autres modèles de souris ghrl-/- déjà décrits au moment de notre étude. Néanmoins, nous observons que l'amplitude des pics sécrétoires de GH des souris ghrl-/- jeunes adultes (7 semaines) est réduite comparée à celle des souris sauvages du même âge. Plus âgées (36 semaines), ces souris retrouvent des profils de sécrétion de GH identiques à ceux des souris sauvages, soulignant un rôle de la ghréline endogène en période de croissance.
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Vora, Aditya. "Long-term effects of neonatal pain on adulthood stress behavior and neuroendocrinology." Diss., Connect to the thesis, 2008. http://hdl.handle.net/10066/1329.
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Lorenzi, Varenka. "The Behavioral Neuroendocrinology of Fish Sex Change: The Role of Steroids and Monoamines." Digital Archive @ GSU, 2009. http://digitalarchive.gsu.edu/biology_diss/76.
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Social status influences reproductive physiology in many species, and sex change in marine teleost fishes provides an excellent model to understand how an organism can modulate its reproductive system in response to social stimuli. The series of experiments presented in this dissertation has focused on the proximate mechanisms underlying sex change and, in particular, the neuroendocrine factors that might translate social information into physiological changes. The bluebanded goby (Lythrypnus dalli) is a sexually plastic fish, and the dominant female typically changes sex when the male is removed from the social group. The direct physical interactions between the male and the females were found to be the main sensory cues that inhibit sex change. Sex steroids can both modulate and be modulated by behavior, and as a result they have been the most obvious candidates for a key role in the regulation of sex change. Males and females showed similar diurnal patterns for steroid hormones, but females had significantly higher water-borne estrogen levels. Concentrations of estradiol, testosterone and 11-ketotestosterone presented sex and tissue differences in brain, gonad and muscle, and they varied in complex ways in different tissues during sex change. The neurotransmitter serotonin (5-HT) has been suggested to be involved in the inhibition of socially regulated sex change because of its role in the modulation of both reproductive and aggressive behavior. None of the pharmacological manipulations performed in L. dalli to alter serotonergic activity was able to overcome the input from the social environment and affect sex change. Neither monoamine levels nor the area or number of 5-HT immunoreactive neurons were different between males, females and sex changers or between dominant and subordinate females. The results do not support the hypothesis of a serotonergic inhibition on sex change in L. dalli, but show that rapid changes in brain androgen levels might be implicated in inducing behavioral or morphological changes associated with sex reversal. Also, steroids respond to changes in the social environment in different ways in different tissues so local steroid synthesis should receive greater attention, and caution is required when using circulating levels to understand behavioral regulation.
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Bosk, Abigail. "Mating induced fos in forebrain neurons of female mice /." Norton, MA : Wheaton College, 2008. http://hdl.handle.net/10090/6013.
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Matthews, Stephen G. "Mechanisms involved in the endocrine response to stress in the sheep." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240089.
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Saelzler, Ursula. "The relationship between basal cortisol levels and cognitive functioning across the adult lifespan." Thesis, Georgia Institute of Technology, 2016. http://hdl.handle.net/1853/55064.
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Age-related declines in cognitive functioning have been well documented, however, there are vast individual differences in the age of onset and magnitude of these changes. This observation has spurred the investigation of the potential risk factors for cognitive decline. Chronic elevations of the steroid hormone cortisol have been shown to compromise hippocampal- and frontal cortex- dependent cognitive tasks in rodents, non-human primates and Cushing’s disease patients. Several studies have extended these findings to investigate possible associations between cortisol and cognition in aging human populations. However, these previous examinations of the role of cortisol in cognitive aging have been hampered by the predominant use of single time-point measures of cortisol, small sample sizes, limited age ranges and/or constrained cognitive testing batteries. The present cross-sectional study investigated the relationship between basal cortisol levels, indexed by a 24-hr free cortisol to creatinine ratio, and cognitive functioning on twelve cognitive outcomes in a sample of 1,853 non-demented adults aged 18 to 93 years. The results showed that elevated cortisol levels had small but significant negative effects on verbal learning and working memory performance across the lifespan and significant negative effects limited to older age on a measure of speeded processing. Longitudinal investigation is warranted to examine if within-person changes in cortisol level predict cognitive change.
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Holtzhausen, Wendy. "Diuretic factors controlling beetle malphighian tubules fluid secretion and immunohistochemistry /." Pretoria : [s.n.], 2006. http://upetd.up.ac.za/thesis/available/etd-07182007-164904.
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Júnior, José Donato. "Estudo da ação do núcleo pré-mamilar ventral de ratos no controle reprodutivo e em respostas à exposição feromonal." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-12032009-181647/.
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O objetivo do presente trabalho foi investigar a relação do núcleo pré-mamilar ventral (PMV): 1) na regulação do sistema reprodutivo em fêmeas, 2) como mediador dos efeitos da leptina e 3) na resposta à estimulação feromonal. Para tanto, induzimos lesão bilateral do PMV em ratas. Foi observado que a lesão do PMV promove: alteração no ciclo estral e da histologia ovariana; redução dos níveis de estradiol e LH; e supressão de vias neurais que controlam o eixo reprodutivo. Além disso, a lesão do PMV impediu que a administração central de leptina induzisse secreção de LH durante o jejum. Em outros experimentos, realizados em ratos machos, verificou-se que neurônios que sintetizam óxido nítrico no PMV e no núcleo medial da amígdala são ativados em resposta ao odor de conspecíficos, em especial o de fêmeas. Assim, foi demonstrado que o PMV exerce papel relevante na regulação do sistema reprodutivo e media a ação estimulatória da leptina na secreção do LH. Além disso, o PMV faz parte do circuito neural relacionado com a resposta aos feromônios.The objective of this study was to assess the role played by the ventral premammillary nucleus (PMV): 1) in the regulation of the female reproductive system, 2) as a mediator of the effects of leptin and 3) in response to pheromonal stimulation. For this purpose, we produced bilateral PMV lesions in female rats. We observed that PMV lesion: disrupted the estrous cycle and altered the number of ovarian antral follicles; reduced the estradiol and LH levels; and suppressed neural pathways that control the reproductive axis. We found that lesions of the PMV blocked leptin stimulation of LH secretion during fasting. In another experiment using male rats, we showed that nitric oxide synthesizing neurons in the PMV and medial nucleus of amygdala are activated by conspecific odors, especially female odors. Thus, we showed that PMV plays an important role in the control of females reproductive system and mediates the stimulatory effects of leptin on LH secretion. Also, PMV is part of the neural circuitry related to pheromonal responses.
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Mir, Bonnín Joan Francesc. "Role of carnitine palmitoyltransferase 1A as a downstream effector of ghrelin in cortical neurons and hypothalamus." Doctoral thesis, Universitat de Barcelona, 2016. http://hdl.handle.net/10803/398850.
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Previous studies have reported the importance of carnitine palmitoyltransferase (CPT) 1A as an essential part of downstream ghrelin signaling in the central nervous system (CNS) for the control of food intake. Lipid metabolism in the ventromedial hypothalamus (VMH) has emerged as a crucial pathway in the regulation of feeding and energy homeostasis. However, the relationship between changes in CPT1A activity and the intracellular downstream effectors in the VMH that contribute to appetite modulation is not fully understood, nor its possible involvement in central extra-hypothalamic functions of ghrelin.
In this work, we examine the effect of long-term expression of a permanently activated CPT1A isoform (CPT1AM) by using an adeno-associated viral vector, injected into the VMH of rats. CPT1AM overexpression produces a sustained increase in food intake which leads to overweight. Mechanistically, CPT1AM alters the lipidomic profile of mediobasal hypothalamus, provoking an increase in ceramides and sphingolipids and a decrease in phospholipids. Furthermore, we detect increased vesicular y-aminobutyric acid transporter (VGAT) and reduced vesicular glutamate transporter 2 (VGLUT2) expressions. These changes are noteworthy, since both GABA and glutamate have been proposed to be mediators in food intake control.
This signature led us to assess the effect of ghrelin in GABAergic neurons. Ghrelin reduces fatty acid oxidation, mitochondrial respiration and mitochondrial reactive oxygen species formation in GT1-7 cells. Moreover, ghrelin produces a reduction in GABA release from primary cortical neurons which is blocked by both pharmacological and genetic inhibition of CPT1A. In addition, ghrelin produces a reduction in: (1) mitochondrial oxygen consumption, (2) citrate and a-ketoglutarate cellular content and (3) GABA shunt connecting TCA cycle and releasable GABA pool.
Taken together, these observations indicate that CPT1A contributes to the regulation of feeding by modulating the expression of neurotransmitter transporters and lipid components that influence the orexigenic pathways in VMH. Moreover, it seems that ghrelin and changes in CPT1A activity modulate mitochondrial function, yielding changes in GABA metabolism, which affect eventually to GABAergic neurotransmission.Estudis previs havien destacat la importància de la carnitina palmitoïltransferasa (CPT) 1A com a part essencial de la senyalització de la grelina al sistema nerviós central (SNC) per al control de la ingesta alimentària. El metabolisme lipídic en el nucli ventromedial de l'hipotàlem (VMH) ha emergit com una via crucial per a la regulació de la ingesta i l'homeòstasi energètica. Això no obstant, la relació entre els canvis en l'activitat de la CPT1A i els efectors intrace•ulars subjacents en el VMH que contribueixen a la modulació de la gana no són totalment compresos, com tampoc la seva involucració en les funcions centrals extrahipotalàmiques de la grelina. En aquest treball, hem examinat l'efecte a llarg termini de l'expressió d'una isoforma mutada permanentment activa de la CPT1A (CPT1AM), fent ús d'un vector víric adeno-associat, injectat en el VMH de rates. La sobreexpressió de la CPT1AM produeix un augment sostingut de la ingesta alimentària que hi promou sobrepès. En la descripció mecanística, la CPT1AM altera el perfil lipidòmic del hipotàlem mediobasal, induint-hi un augment de ceramides i esfingolípids i alhora una reducció en fosfolípids. A més a més, hem detectat un augment en les expressions del transportador vesicular de l'àcid y-aminobutíric (GABA) (VGAT, en les seves sigles en anglès) i una reducció del transportador vesicular de glutamat 2 (VGLUT2, en les seves sigles en anglès). Aquests canvis són destacables, ja que tant GABA como glutamat han sigut proposats com a mediadors en el control de la ingesta alimentària. Aquestes observacions ens dugueren a estudiar l'efecte de la grelina en neurones GABAèrgiques. La grelina redueix l'oxidació d'àcids grassos, la respiració mitocondrial i la formació d'espècies reactives d'oxigen en cèl•lules GT1-7. D'afegitó, la grelina produeix una reducció en l'alliberament de GABA de neurones corticals primàries, la qual cosa és blocada tant per inhibició genètica i farmacològica de la CPT1A. A més a més, la grelina hi produeix una reducció: (1) del consum mitocondrial d'oxigen, (2) del contingut cel•lular de citrat i d'a-cetoglutarat i (3) de la via de desviació de GABA que connecta el cicle dels àcids tricarboxílics i el contingut alliberable de GABA. En conjunt, aquestes observacions indiquen que la CPT1A contribueix a la regulació de la ingesta amb la modulació de l'expressió de transportadors involucrats en la neurotransmissió i la modulació de components lipídics que influencien les vies orexigèniques del VMH. A més a més, sembla que la grelina i els canvis en l'activitat CPT1A modulen la funció mitocondrial, obtenint-ne canvis al metabolisme del GABA, que afecten en darrera instància a la neurotransmissió GABAèrgica.
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Spencer, Sarah J. "Stress and the brain : role of the medial prefrontal cortex in regulation of the hypothalamic-pituitary-adrenal axis /." [St. Lucia, Qld.], 2004. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe18148.pdf.
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Amstalden, Marcel. "Role of leptin in regulating the bovine hypothalamic-gonadotropic axis." Diss., Texas A&M University, 2003. http://hdl.handle.net/1969.1/507.
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The physiological mechanisms through which nutrition mediates its effects in controlling reproduction are not well characterized. Both neural and endocrine components have been implicated in the communication of nutritional status to the central nervous system. Leptin, a hormone synthesized and secreted mainly by adipocytes, is heavily involved in this communication network. The objectives of studies reported herein were 1) to determine the effects of short-term restriction of nutrients on circulating leptin, leptin gene expression in adipose tissue, and leptin receptor (LR) gene expression in the adenohypophysis of ovariectomized cows; and 2) to investigate the responsiveness of the hypothalamic-adenohypophyseal (AP) axis of fasted and non-fasted cattle to leptin. Studies demonstrated that circulating concentrations of leptin and leptin gene expression in subcutaneous adipose tissue are decreased by fasting. Although 2 to 3 days of fasting did not affect patterns of release of luteinizing hormone (LH), cerebroventricular infusions of leptin increased mean circulating concentrations of LH in fasted, but not normal-fed cows, without affecting frequency or amplitude of pulses of LH. In vitro studies were conducted to determine whether the in vivo effects of leptin could be accounted for at the hypothalamic and/or AP levels. Leptin did not affect the release of gonadotropin-releasing hormone (GnRH) from hypothalamic-infundibular explants from either normal-fed or fasted cattle. Moreover, leptin did not affect the basal release of LH from bovine AP cells or AP explants from normal-fed cows. However, leptin induced a higher basal release of LH from AP explants of fasted cows and increased GnRH-stimulated release of LH from AP explants of normal-fed cows. Results demonstrate that leptin acts directly at the AP level to modulate the secretion of LH, and its effects are dependent upon nutritional status. Cellular mechanisms associated with the increased responsiveness of gonadotropes to leptin in fasted cows were investigated. Expression of LR and suppressor of cytokine signaling-3 (SOCS-3) in the adenohypophysis did not account for the increased responsiveness of fasted cows to leptin. Therefore, although leptin clearly stimulates the hypothalamic-gonadotropic axis in nutrient-restricted cattle, it is unclear why cattle maintained under neutral or positive energy balance are resistant to leptin.
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Branco, Ricardo Garcia. "Stress response in critically ill children." Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609718.
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Beck, Meredith Nell. "Effects of Prolactin on the Hypothalamic Pituitary Adrenal Axis in Postpartum Female Rats." Miami University Honors Theses / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=muhonors1303497697.
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Soori, Mehrnoosh. "Neuroendocrine differentiation of prostate cancer cells a survival mechanism during early stages of metastatic colonization of bone /." Access to citation, abstract and download form provided by ProQuest Information and Learning Company; downloadable PDF file, 105 p, 2009. http://proquest.umi.com/pqdweb?did=1654490661&sid=6&Fmt=2&clientId=8331&RQT=309&VName=PQD.
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Altmieme, Zeinab. "The Role of Nonapeptides in Male Reproduction in Two Cyprinid Species, the Zebrafish (Danio rerio) and the Goldfish (Carassius auratus)." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/38911.
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Two distinct nonapeptide systems, consisting of the vasotocin- and oxytocin-related peptides have evolved in vertebrates, and their role in male reproduction is well-described in mammals. In contrast, their comparative role in reproduction in basal vertebrate species, and teleost fishes in particular, has not been investigated in great detail. Using two cyprinid species, the zebrafish (D. rerio) and the goldfish (C. auratus), I address the hypothesis that the teleost nonapeptides vasotocin and isotocin stimulate male cyprinid reproductive physiology by affecting central neuronal and/or peripheral endocrine pathways.
To test this hypothesis in zebrafish, an indeterminate breeder, I conducted pharmacological inhibition experiments employing vasotocin and isotocin-specific antagonists in males, a treatment predicted to inhibit reproductive success in mating trials. Because nonapeptides can act both as central peptide neuromodulators and as secreted hormone, I further quantified indices of male courtship behavior (nudging, circling and chasing) and major androgens (testosterone and 11-keto-testosterone) as key endocrine indices of the male reproductive axis. Together, these experiments revealed a dose-dependent, differential inhibition of spawning success, with significant reductions (-65%) in egg fertilization rate observed in pairs in which males had been i.p. injected with 5 ng/g vasotocin and significant reductions (-79%) observed at 500 ng/g i.p injected isotocin. In either case, these partial inhibitions of reproductive success were correlated with significant decreases in specific indices of male courtship behavior, but not endocrine indices, suggesting that individual nonapeptides mediate their effects via central modulation of behavioural neurocircuits. Interestingly, a co-administration of vasotocin and isotocin antagonists completely abolished reproductive success, however this effect was neither correlated with decreases in male courtship behavior, nor endocrine indices, suggesting a separate mode of action, possibly at the level of male pheromone release. To further probe the role of nonapeptides in male zebrafish reproduction, I subsequently tested the hypothesis that nonapeptide systems are acutely activated by key reproductive cues, specifically the releaser pheromone PGF2α, which serves as a chemoattractant and acutely stimulates male reproductive behavior in male cyprinids. Using a chemoattractant choice assay in conjunction with immunohistochemistry and gene expression approaches, I determined whether male zebrafish are attracted to pheromonal cues and acutely activate isotocinergic neurons in the short term and/or regulate nonapeptide gene expression in the longer term. My results show that individual male zebrafish are attracted to PGF2α in an acute choice test. Furthermore, an increase in p-ERK immunoreactivity, a marker of neuronal activation, was observed in the olfactory bulb 10 min following exposure, suggesting a specific response to the pheromone compared to EtOH vehicle. However, no co-localization of p-ERK and IT-positive perikarya was observed in the preoptic area (POA), refuting the hypothesis that PGF2α exposure acutely activates isotocinergic neurons in zebrafish. Analysis of whole brain relative mRNA transcript abundance revealed that PGF2α exposure time-dependently regulates whole brain isotocin, but not vasotocin transcript abundance, suggesting secondary longer-term effects of PGF2α exposure on the isotocinergic system.
Using an analogous experimental approach, I further tested the hypothesis that nonapeptides stimulate male reproductive physiology in goldfish, a determinate breeder. Sexually mature male goldfish pretreated with saline or vasotocin or isotocin antagonists were exposed to saline or PGF2α-injected stimulus females and male courtship behavior (chasing, circling), endocrine indices (circulating testosterone) and milt release were quantified. Both nonapeptide antagonists reduced strippable male milt quantity in response to PGF2α-injected females, suggesting a neuronal or hormonal action of both nonapeptides on goldfish milt release.
Together, I show that nonapeptides contribute to male reproductive physiology in two species of cyprinids with different reproductive tactics. However, the mode of action may differ from one species to another, with evidence suggesting that nonapeptides play a role in the regulation of reproductive behavior and, possibly, male pheromone, release in zebrafish, while effects on male goldfish seem to be exclusively related to the release of milt. Future studies should compare other teleost species with specific reproductive biology and focus on the gonadal roles of nonapeptides in sperm maturation and/or release.
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Saleh, Nadine. "Troubles hormonaux et leur implication dans la progression de la maladie de Huntington." Thesis, Paris Est, 2009. http://www.theses.fr/2009PEST0061.
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Les processus physiopathologiques qui mènent à la dégénérescence neuronale ainsi qu’aux symptômes de la maladie de Huntington (MH) demeurent non identifiés et les hypothèses actuelles ne permettent pas d’expliquer l’hétérogénéité intra et interindividuelle de l’évolution de ces symptômes. Ainsi, la progression de la maladie reste donc difficile voire impossible à prédire. Dans ce contexte, il est important d’explorer d’autres facteurs qui semblent être impliqués dans le processus pathogène de la maladie mais qui pourraient également influencer l’évolution de ces symptômes et ainsi prédire la progression de la maladie. Plusieurs éléments de preuve renforcent l’hypothèse de l’existence de troubles hormonaux dans la MH tels que l’atteinte de l’hypothalamus et la perte de poids. Cependant, en raison du peu d’études, de leur qualité et de la discordance de leurs résultats, l’existence des modifications hormonales dans la maladie de Huntington et plus particulièrement leur lien avec la progression de la maladie reste controversée. L’objectif de ce travail est de décrire le profil hormonal de l’axe hypothalamohypophysaire dans la MH afin de mieux comprendre le rôle de ces hormones sur la progression et éventuellement sur la physiopathologie de la maladie. Dans notre étude transversale, nous avons mis en évidence une activation de l’axe somatotrope (Growth Hormone/Insulin Growth Factor 1), une inhibition en fonction de la sévérité de la maladie de deux axes : gonadotrope (Testostérone) et thyréotrope (Thyroid Stimulating Hormone et triiodothyronine) mais aucune modification des hormones de l’axe corticotrope ni de la prolactine. De plus, la modification hormonale de l’axe somatotrope était non pathologique et précoce alors qu’elle était tardive pour les deux autres axes. Pour expliquer le lien entre ces modifications et la progression de la maladie une étude longitudinale a été mise en place. Les résultats de cette étude montre que seule l’élévation plasmatique d’IGF1 était prédictive de la détérioration cognitive. L’ensemble de nos résultats apporte une meilleure description et compréhension du profil de l’axe hypothalamo-hypophysaire dans la maladie de Huntington. Les axes pituitaires ne sont pas tous atteints et leur atteinte n’est pas dans le même sens. La relation inverse entre l’activation de l’axe somatotrope et la détérioration cognitive renforce l’hypothèse d’une résistance à l’effet de l’IGF1 dans la maladie de Huntington comme pour la maladie d’alzheimer. En conclusion, compte tenu de l’implication de l’IGF1 dans la prédiction de la progression cognitive dans la maladie de Huntington, il serait intéressant de détecter si les modifications biologiques de l’IGF1 existent dès la phase asymptomatique cognitive afin d’envisager d’utiliser l’IGF1 comme biomarqueur de l’apparition ou de l’évolution des symptômes cognitives. D’un autre côté, il serait important d’étendre les recherches sur les mécanismes responsables des modifications hormonales dans la maladie de Huntington afin de mieux comprendre l’effet de cause à effet s’il existe entre ces modifications et les symptômes de la maladieThe pathophysiological processes leading to neurodegeneration and the symptoms of Huntington's disease (HD) remain unidentified and current hypothesis do not explain the intra and interindividual heterogeneity of the evolution of these symptoms. Thus, the progression of the disease remains difficult or impossible to predict. In this context, it is important to explore other factors that appear to be involved in the pathogenic process of the disease but could also influence the evolution of these symptoms and predict disease progression. Several evidences reinforce the hypothesis of the existence of hormonal disorders in HD such as the atrophy of the hypothalamus and weight loss. Because of few studies, their quality and the discrepancies of their results, the existence of hormonal changes in Huntington's disease and particularly their relationship to disease progression remains controversial. The objective of this work is to describe the hormonal profile of the hypothalamicpituitary axis in HD in order to better understand the role of these hormones on the progression and on the pathophysiology of the disease. In our cross-sectional study, we identified an activation of the somatotropic axis (Growth Hormone / Insulin Growth Factor 1), an inhibition according to the severity of the disease in two axes: gonadotrope (Testosterone) and thyréotrope (Thyroid Stimulating hormone and triiodothyronine) but no change in hormones of corticotropic axis and prolactin. In addition, the somatotropic axis is overactive even in patients with early disease. To explain the link between these changes and the progression of the disease, a longitudinal study was done. The results of this study showed that only the elevated plasma IGF1 was predictive of cognitive impairment. All of our results provide a better description and understanding of the profile of the hypothalamic-pituitary axis in Huntington's disease. Pituitary axes are not all disturbed. The inverse relationship between activation of the somatotropic axis and cognitive impairment strengthens the hypothesis of a resistance to the effect of IGF1 in Huntington's disease like in Alzheimer's disease. In conclusion, given the involvement of IGF1 in the prediction of cognitive progression in Huntington's disease, it would be interesting to detect whether the biological changes of IGF1 are already present at the asymptomatic cognitive stage in order to use IGF1 as a biomarker of the onset or changes in cognitive symptoms. On the other hand, , it would be important to extend research on the mechanisms responsible for hormonal changes in Huntington's disease to better understand the link between these changes and symptoms of the disease
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Clarkson, Jenny, and 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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Mimouni, Nour El Houda. "Elevated prenatal anti-Müllerian hormone reprograms the fetus and induces polycystic ovary syndrome (PCOS) in adulthood." Thesis, Lille, 2019. http://www.theses.fr/2019LILUS051.
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Le syndrome des ovaires polykystiques (SOPK) est la principale cause d’infertilité feminine à travers le monde, associé à un risqué élevé de comorbidités avec des conséquences économiques non négligeables. Ce syndrome est caractérisé par une oligo-anovulation, une hyperandrogénie, et un aspect échographique d’ovaires polykystiques. De plus, la plupart des femmes atteintes de SOPK présentent des concentrations élevées de LH suggérant une libération accrue de GnRH. De plus, les patientes SOPK ont habituellement des concentrations en Hormone Anti Müllerienne (AMH) 2 à 3 fois plus élevés que les femmes non atteintes.Alors que l’origine exacte du SOPK demeure inconnue, des études de clustering familial et portant sur des jumeaux ou des ascendants de femmes atteintes du SOPK ont mis en évidence une forte composante héréditaire. Cependant, les gènes candidats identifiés n’expliquent qu’à peine 10% des cas de SOPK suggérant qu’une origine développementale et que des facteurs environnementaux tels que des modifications hormonales durant la vie foetale pourrait être à l’origine du SOPK.Dans cette étude, nous avons d'abord comparé les concentrations d'AMH dans un groupe de femmes atteintes de SOPK et chez des femmes témoins pendant la grossesse. Les concentrations d’AMH se sont révélées significativement plus élevées chez les SOPK par rapport aux témoins. Nous avons ensuite utilisé ces résultats cliniques pour développer un modèle animal murin de SOPK en exposant les souris gestantes à une concentration élevée d’AMH au cours d'une fenêtre temporelle spécifique. Nous avons montré que cette exposition foetale conduisait à une cascade d'altérations affectant le cerveau maternel, les ovaires et le placenta, entrainant une reprogrammation du cerveau foetal et induisant l'acquisition des principaux critères diagnostiques retrouvés dans le SOPK, à savoir l'hyperandrogénie, l'augmentation de la pulsalitié de la LH et de l'oligo-anovulation, ainsi qu’une augmentation persistante de l'activité électrique de la GnRH à l'âge adulte. De plus, nos résultats montrent que les conséquences à long terme d'une exposition courte à des niveaux élevés d'AMH pendant la gestation s'étendent au-delà de la première génération exposée et que les manifestations de type SOPK semblent être transmises d’une génération à l’autre chez les femelles.De manière intéressante, en utilisant une approche pharmacologique, nous avons démontré que l’inhibition partielle de la voie de signalisation de la GnRH permettait de restaurer chez les animaux SOPK un phénotype neuroendocrinien normal, en rétablissant des concentrations hormonales normales, la cyclicité oestrale et leur morphologie ovarienne.Enfin, nous avons cherché à comprendre comment une exposition précoce à un excès d'AMH affecterait les caractéristiques neuroendocriennes et reproductives de la progéniture mâle. Ici, nous avons démontré que le traitement par AMH en période prénatale modifiait la fonction de l'axe hypothalamo-hypophyso-gonadique (HPG) chez les mâles, qui ne parviennent pas à engager le pic de testostérone néonatal normalement observé chez les nouveau-nés mâles témoins, conduisant à une féminisation des circuits sexuellement dimorphiques cérébraux, à une augmentation de la LH, et finalement à une diminution drastique des niveaux de testostérone à l’âge adulte, à des altérations sévères de la stéroïdogenèse et de la spermatogenèse ainsi qu'à un risque plus élevé de développer une cryptorchidie à l'âge adulte. Ainsi, il pourrait être intéressant de relier les résultats de cette étude au phénotype reproductif des garçons de femmes atteintes du SOPK, qui ont été exposés pendant la grossesse mais qui ne sont habituellement pas suivis plus tard à l'âge adulte [...]Polycystic ovary syndrome (PCOS) is the main cause of female infertility worldwide with high comorbidity and economic burden. It is mainly characterized by hyperandrogenism, oligo/anovulation and polycystic appearing ovaries. Moreover, most women with PCOS exhibit higher levels of circulating luteinizing hormone (LH), suggestive of heightened gonadotropin-releasing hormone (GnRH) release. Additionally, PCOS patients also exhibit 2-3x higher levels of Anti-Müllerian Hormone (AMH) as compared to healthy controls.While the exact origin of PCOS is unknown, familiar clustering and twin studies of PCOS patients and their relatives suggest a strong heritable component in PCOS. However, the candidate genes identified account for only <10% of the estimated 70% heritability of PCOS, implying that it may originate during intrauterine development and that environmental factors, such as hormonal imbalances during fetal life, could be involved in the onset of PCOS.In this study, we first measured AMH levels in a cohort of pregnant women with PCOS and control women which revealed that AMH is significantly more elevated in the former group versus the latter, we then modelized our clinical findings by exposing pregnant mice to high concentration of AMH during a specific temporal window and showed that this fetal exposure leads to a cascade of alterations impacting the maternal brain, the ovaries, and the placenta, which consequently reprogram the fetal brain and induce the acquisition of the major PCOS cardinal neuroendocrine reproductive features, namely hyperandrogenism, elevation in LH pulse frequency and oligo-anovulation, and a persistent rise in the GnRH neuronal firing activity in adulthood. Moreover, our results show that the long-term consequences of a short exposure to elevated AMH levels during gestation expand beyond the first generation exposed and that PCOS-like manifestations seem to be transmitted across subsequent generations of females.Intrestingly, using a pharmacological approach, we demonstrate that tempering GnRH signaling pathway rescues the neuroendocrine phenotype of PCOS-like animals, restoring their normal hormonal levels, estrus cyclicity and ovarian morphology.Lastly, we sought to understand how early exposure to AMH excess would affect the neuroendocrine and reproductive features of the male offspring. Here, we demonstrate that prenatal AMH treatment profoundly impacts the Hypothalamic-Pituitary-Gonadal (HPG) axis function in males, which fail to engage the testosterone surge at birth observed in control newborns, leading to a feminization of sexually dimorphic circuitries of their brains, an increase in LH, a drastic decrease in testosterone levels, severe alterations in the testicular steroidogenesis and morphology as well as a higher risk of developing cryptorchidism in adulthood. Thus, it could be of clinical interest to relate findings from this study to the reproductive phenotype of sons of PCOS women, who are exposed during gestation but not systematically investigated in adulthood.Collectively, our results challenge the concept of PCOS originating in utero and appear to consolidate the role of AMH as a trigger of the pathogenesis, suggesting that an altered hormonal milieu during early life associated with PCOS may not only affect the female fetus but also the male fetus exposed and that these alterations could be transmitted across multiple generations.These findings point to PAMH mouse model as an excellent preclinical tool to investigate both neuroendocrine disturbances of PCOS and how developmental programming effects are transmitted, while offering a therapeutic avenue for the treatment of the disease
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Mennigen, Jan A. "The Serotonergic System as a Target for Neuroendocrine Disruption in the Brain of Goldfish (Carassius auratus)." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19927.
Full textAbstract:
Serotonin stimulates reproduction and inhibits feeding/growth in the neuroendocrine brain of goldfish. The objective of this thesis is to study the effects of selective serotonin
reuptake inhibitor pharmaceuticals (SSRIs) on these systems, as SSRIs, such as fluoxetine, are detected in effluent and bioconcentrate in the brain of wild fish. Genes of the serotonin system were cloned to identify molecular conservation, seasonal expression, and tissue distribution. The serotonin transporter, the target molecule of fluoxetine, was highly conserved and ubiquitously expressed in goldfish. Seasonal changes of hypothalamic gene expression of the serotonin transporter support a role in the seasonal modulation of both processes. Fluoxetine injection experiments were used to assess effects on reproductive endpoints and to identify molecular mechanisms in the neuroendocrine brain. Fluoxetine inhibited serum estradiol concentrations in female goldfish and decreased isotocin mRNA abundance in the hypothalamus and telencephalon. Isotocin injections stimulated circulating estradiol concentrations, providing a causal link. Evidence for an involvement of serotonin in isotocin regulation was investigated using immunocytochemistry and 5-HT1A receptor agonists and antagonists. A close proximity of
serotonin fibers and isotocin cell bodies and fibers was found in the telencephalon and pituitary,respectively. Injection of a 5-HT1A receptor antagonist inhibited isotocin mRNA expression in the telencephalon. Identified gene targets were investigated in waterborne fluoxetine exposures,including environmental concentrations. Waterborne fluoxetine led to a reduction in basal and pheromone-stimulated milt volume in male goldfish. Gene expression evidence indicated a central inhibitory effect of fluoxetine through the decrease in mRNA abundance of follicle-stimulating hormone in the pituitary and isotocin in the telencephalon. Feeding rate and weight decreased in fluoxetine-injected goldfish, indicating an anorexigenic effect. Fluoxetine induced changes in the gene expression of the feeding peptides neuropeptide Y, corticotropin-releasing factor, and cocaine- and amphetamine-regulated transcript-I in the hypothalamus and telencephalon. Waterborne exposure to fluoxetine validated the anorexigenic effect in goldfish and was correlated with increased expression of corticotropin-releasing factor mRNA, an anorectic peptide. The thesis provides evidence for disrupting effects of fluoxetine on neuroendocrine control of reproductive
function and feeding/growth in goldfish, partially at environmental concentrations. The thesis provides the framework for the investigation of existing aquatic contaminants which modulate the serotonin system.
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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.
Full textAbstract:
The plasma membrane electrical activities of neurons that secrete gonadotropin releasing
hormone (GnRH), referred to as GnRH neurons hereafter, have been studied extensively.
A couple of mathematical models have been developed previously to explain different
aspects of these activities including spontaneous spiking and responses to stimuli such as current injections, GnRH, thapsigargin (Tg) and apamin. The goal of this paper is to
develop one single, minimal model that accounts for the experimental results reproduced
by previously existing models and results that were not accounted for by these models.
The latter includes two types of membrane potential bursting mechanisms and the
associated calcium oscillations in the cytosol. One of them has not been reported in
experimental literatures on GnRH neurons and is thus regarded as a model prediction.
Other improvements achieved in this model include the incorporation of a more detailed
description of calcium dynamics in a three dimensional cell body with the ion channels
evenly distributed on the cell surface. Although the model is mainly based on data
collected in cultured GnRH cell lines, we show that it is capable of explaining some
properties of GnRH neurons observed in several of other preparations including mature
GnRH neurons in hypothalamic slices. One potential explanation is suggested. A
phenomenological reduction of this model into a simplified form is presented. The
simplified model will facilitate the study of the roles of plasma membrane electrical
activities on the pulsatile release of GnRH by these neurons when it is coupled with a
model of pulsatile GnRH release based on the autoregulation mechanism.
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TAMASHIRO, KELLIE L. K. "CHRONIC SOCIAL STRESS EFFECTS ON ENERGY HOMEOSTASIS: TOWARDS AN ANIMAL MODEL OF THE METABOLIC SYNDROME." University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1120014027.
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Medrado, Andreone Teles. "An Atlas of catfish brain - Steindachneridion parahybae (Teleostei: Siluriformes): a detailed cytoarchitectonic study of the different brain areas and nuclei as a basis for further morphological and functional studies." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/41/41135/tde-04112015-150105/.
Full textAbstract:
In the present Master\'s Dissertation, a detailed cytoarchtectonic study of the brain of the juvenile catfish - Steindachneridion parahybae, has been performed. The animals used for this Atlas were juvenile specimens of one hundred days post-fertilization. The coronal (transverse) sections (5µm-thick) were obtained by using a rotary microtome, stained with cresyl-violet and examined under a photomicroscopy with the help of a digital system of analysis. Some criteria have been used to classify the different cell masses of the catfish brain: (i) characteristic size, shape and intensity of the staining from the perykarya; (ii) packing density and distribution pattern of the cell bodies; (iii) neuropil surrounding the cell groups and (iv) consistency of cell groups in both hemispheres and different brains of catfish. Thus, around one hundred and thirty nuclei have been described in the catfish brain, which are distributed in four main region that are from rostral to caudal: telencephalon, diencephalon, mesencephalon and rhombencephalon. Although we have observed important similarities between the brain of catfish and other teleosts, we have also noticed some differences in the characteristics and placement of several nuclei in relation to other teleosts, or even when compared to the brain of species of the same Order, the Siluriformes. Some of these differences could be related with the age of the animals studied here, but probably represent species-specific differences because the brain of adult catfish specimens has a great similarity in cytoarchitecture and overall organization compared to younger animals. The main outcome of this study has been the availability of a complete Atlas of the brain of catfish, which has been used to localize precisely the distribution of cells and fibers of the Gonadotropin-releasing hormone in the brain. This Atlas will also represent a valuable tool for future endocrine analyses, allowing the precise mapping of the different neurohormones in the brain of catfish, as well as for the study of neural connections among different brain areasEsta Dissertação de Mestrado, apresenta-se estruturalmente como um Atlas, em que é apresentado um detalhado estudo citoarquitetônico do encéfalo de catfish- Steindachneridion parahybae. Para a realização deste, foram utilizados 7 juvenis de 100 dias após a eclosão, analisados por técnicas rotineiras de histologia, cujas secções coronais(transversais) - 5&um;m de espessura-, foram obtidas utilizando-se de um micrótomo rotativo, coradas com violeta de cresil e examinadas a partir de sistema digital de análise. Alguns critérios foram utilizados para classificar as diferentes massas de células do cérebro catfish, tais como: (i) o tamanho característico, forma e intensidade da coloração do pericário; (ii) padrão de densidade de agrupamento e distribuição dos corpos celulares; (iii) a presença de neurópilos ao redor dos desses agrupamentos celulares e (iv) a consistência/coerência destes agrupamentos em ambos os hemisférios dos diferentes encéfalos, então analisados. Dessa forma, são descritos aproximadamente130 massas celulares para o encéfalo de S. parahybae, as quais estão distribuídas em quatro principais regiões que, da parte rostral para caudal, são: telencéfalo, diencéfalo, mesencéfalo e rombencéfalo. Embora são observadas semelhanças entre o cérebro de S. parahybae e de outros teleósteos, nota-se, também, certas diferenças quanto às características e/ou localização das massas celulares em relação ao encéfalo de outros teleósteos, ou mesmo quando comparado com o cérebro de espécies da mesma ordem, Siluriformes. Algumas destas diferenças pode estar relacionada com a idade dos animais estudados, no entanto,também podem representar diferenças espécie-específicas, uma vez que o encéfalo adultos de S. parahybae apresentam grande similaridade citoarquitetônica, além da organização geral do encéfalo, previamente observadas em animais acima dos 100 dias após a eclosão. Portanto, como resultado deste estudo tem-se a disponibilidade de um Atlas completo do encéfalo de S. parahybae, o qual representa uma ferramenta valiosa para o estudo das conexões neurais entre diferentes áreas do encéfalo, bem como para futuras análises endócrinas, permitindo o mapeamento preciso de neuro-hormônios nesta espécie, como demonstrado ao longo deste estudo, para o hormônio liberador de gonadotropinas
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Latsko, Maeson Shea. "CORTICOSTERONE TREATMENT PROVIDES PROTECTION INTO ADULTHOOD FROM THE ADVERSE EFFECTS OF ADOLESCENT SOCIAL DEFEAT." Kent State University / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=kent153251170904353.
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Silva, Renata Juliana da. "Efeitos do treinamento físico intenso e da restrição alimentar sobre a ação da leptina mediada pelo hormônio concentrador de melanina no eixo reprodutor de ratas." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/42/42131/tde-09022012-121522/.
Full textAbstract:
Avaliamos o efeito do treinamento físico intenso e da restrição alimentar no eixo reprodutor e na expressão do RNAm do MCH em ratas fêmeas. Utilizamos ratas fêmeas sedentárias alimentadas (SA), sedentárias com restrição alimentar, treinadas alimentadas (TA) e treinadas com restrição alimentar. O grupo TR entrou em anestro a partir da quarta semana de experimento. Os grupos restritos apresentaram redução de peso corporal, ovários, úteros e tecido adiposo branco, comparados aos alimentados. Houve redução sérica de leptina nos grupos SR e TR. Os grupos TA, SR e TR apresentaram cistos ovarianos. A expressão do RNAm do ppMCH na área incerto-hipotalâmica (IHy) foi menor nos animais TR, SR e nos animais alimentados em proestro, e na área hipotalâmica lateral (LHA) foi maior nos animais em restrição alimentar e nos animais alimentados em proestro. Conclui-se que a leptina exerce forte influencia no eixo reprodutor feminino, tal ação parece ter envolvimento do MCH, sobretudo o proveniente da IHy, uma vez que o MCH da LHA tem relação com o estímulo a busca de alimento.We evaluated the effect of intense physical training and food restriction on the reproductive axis and MCH mRNA expression in female rats. We used female rats fed sedentary (SF), food-restricted sedentary, trained fed (TF) and trained with food restriction. The group entered anestrus TR from the fourth week of the experiment. The restricted groups had reduced body weight, ovary, uterus and white adipose tissue, compared to the fed. There was a reduction of serum leptin in the SR and TR groups. The TF groups, SR and TR had ovarian cysts. The expression of mRNA ppMCH incerto-hypothalamic area (IHy) was lower in TR animals, SR and animals fed on proestrus, and the lateral hypothalamic area (LHA) were higher in animals on restricted food and animal feeding in proestrus. It is concluded that leptin exerts a strong influence on female reproductive axis, such action appears to have involvement of MCH, especially from the IHy, since the MCH of the LHA is related to the motivational behavior associated to the search for food.
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Höglund, Erik. "Neuroendocrinology of agonostic interaction and social signalling in Artic charr (Salvelinus alpinus) : Studies on the neuroendocrine regulation of aggressive behaviour, stress responses and skin colour." Doctoral thesis, Uppsala University, Department of Evolutionary Biology, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-616.
Full textAbstract:
This thesis shows that socially subordinate Arctic charr (Salvelinus alpinus) display elevated brain serotonergic (5-HT) and norepinephric activity along with a chronic activation of the hypothalamic-pituitary-interrenal (HPI) axis, including elevated plasma concentrations of á-MSH. Furthermore, subordinate fish showed an inhibition of aggressive behaviour and darker body coloration, skin darkness being positively correlated with plasma á-MSH. Fish kept on dark background, and thus being darker in body colour, were less aggressive than conspecifics interacting on white background, supporting the hypothesis that skin darkening could signal social submission. The 5-HT1A -receptor agonist 8-OH-DPAT stimulated HPI axis activity in non-stressed fish, but if administrated to stressed fish it inhibited HPI axis activity, suggesting that 5-HT1A receptors may act as both post- and pre-synaptic receptors. 8-OH-DPAT also induced skin darkening in both non-stressed and stressed fish. Stimulation of brain dopaminergic activity by L-dopa treatment counteracted the stress-induced inhibition of aggressive behaviour, and stress related effects on brain 5-HT activity and plasma levels of cortisol. In conclusion, social subordination in Arctic charr results in skin darkening and an inhibition of aggressive behaviour. Stress-induced effects, that could be mediated by elevated brain 5-HT activity, and serve as a way of signalling social position and coping with stress.
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Höglund, Erik. "Neuroendocrinology of agonistic interaction and social signalling in Arctic charr (Salvelinus alpinus) : studies on the neuroendocrine regulation of aggressive behaviour, stress responses and skin colour /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4964-6/.
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Lee, Yoojin. "Testosterone Reactivity and Neural Activation in the MID task." ScholarWorks@UNO, 2014. http://scholarworks.uno.edu/td/1930.
Full textAbstract:
The purpose of the project was to determine if testosterone reactivity and neural changes could be observed in response to a reward-seeking competitive task, respectively, and whether testosterone was related to neural activation. Forty nine undergraduate students were recruited playing the Monetary Incentive Delay (MID). We found that a subset of participants (N=20) showed testosterone reactivity to the task (ps < .05). During the EEG analyses, cue had a main effect on FRN amplitude in a trend level (p = .084): The large incentive cue triggered smaller (less negative) FRN amplitude than the small incentive cue did (p < .05), especially during the second reward seeking block (A’) (p = .065) and especially within males (p < .05). Testosterone level and reactivity were not further associated with FRN amplitude (ps > .1). Taken together, results show both testosterone and FRN amplitude may be sensitive to a complex reward-seeking and competition.
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Weil, Zachary M. "Social And Temporal Determinants Of Brain, Behavior And Immune Function." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1219085420.
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Sacchi, Federico. "Glutamatergic Regulation of Adult Goldfish Radial Glial Cells Via Group III Metabotropic Glutamate Receptors." Thesis, Université d'Ottawa / University of Ottawa, 2018. http://hdl.handle.net/10393/38535.
Full textAbstract:
Aromatase is an enzyme that converts androgens to estrogens. In teleosts, brain aromatase, also known as aromatase B (cy19a1b), is only expressed in radial glial cells (RGCs). This is in contrast to aromatase A, which is expressed in gonads. Estrogens such as estradiol (E2) modulate neurogenesis in the adult teleost brain. Recent studies show that E2 also differentially regulates aromatase B expression in goldfish RGCs. As a result, teleost RGCs are suggested to be involved in regulating neurogenesis. In addition, aromatase B expression in goldfish RGC is under the control of dopamine suggesting that neurons and neurotransmitters can regulate RGC function. Interestingly, goldfish RGC transcriptome data shows the expression of one group of metabotropic glutamate receptors (mGluRs), group III mGluRs, which suggests that glutamate may affect RGC function. In this thesis, I present my findings regarding potential glutamatergic regulation of RGCs. Firstly, I investigated the distribution of glutamatergic synaptic vesicles and RGCs in the female goldfish forebrain. Double-staining immunohistochemistry shows that vesicular glutamate transporter (vGLUT) 1/2-labelled glutamatergic synaptic vesicles are in close anatomical proximity to aromatase B-labelled RGCs, which suggests potential regulation of RGCs by glutamate. Glutamatergic regulation of cyp19a1b, cyclin D1 (ccnd1), cyclin A2 (ccna2), mGluR6b (grm6b), mGluR7 (grm7), and mGluR8b (grm8b) expression in cultured adult female goldfish RGCs was also examined. Results from pharmacological manipulations and qPCR data analysis show that selective activation of group III mGluRs decreased cyp19a1b, ccnd1, and ccna2 mRNA via inhibition of cAMP/PKA signalling. Furthermore, grm7 mRNA is positively regulated by cAMP-dependent signalling. The glutamate analog L-glutamic acid decreased cyp19a1b mRNA and increased ccnd1 and grm6b mRNA in a dose-dependent manner. This suggests that ccnd1 and grm6b expression may be regulated by glutamate receptors other than group III mGluRs, for example, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, which are expressed in cultured goldfish RGCs. It was found that E2 upregulated cyp19a1b, ccnd1 and grm7 mRNA. However, selective activation of group III mGluRs decreases the stimulatory effect of E2 on ccnd1 expression. My findings show that glutamate finely regulates RGC neurogenic and steroidogenic genes, which may implicate glutamate in the regulation of RGC differentiation, RGC proliferation, and neurogenesis in surrounding cells.
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Waye, Andrew. "An Investigation of Pulp Mill Effluents and Their Wood Feedstocks as Potential Neuroendocrine Disruptors of the Fish Reproductive Axis." Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/32145.
Full textAbstract:
Common observations of reduced gonad size and spawning inhibition in wild and laboratory raised fish exposed to pulp mill effluents indicate that reproductive neuroendocrine signalling pathways may be upset. This thesis supported the neuroendocrine disruption of reproduction hypothesis by identifying potential disruptors and targets where these impacts may occur. A mechanistic study of the in vivo fathead minnow (FHM) spawning assay used by industry to assess effluent quality showed that ovulation, but not milt production, was impaired. This finding supported the hypothesis that the neuroendocrine cascade that triggers ovulation may be disrupted. I hypothesized that neuroactive constituents previously described in effluents were originating in wood feedstocks and neuroactive extracts of hardwood and conifer feedstocks were identified. Phytochemicals associated with effluents were neuroactive. Structurally similar phenolic phytochemicals showed monoamine oxidase (MAO) inhibition, and resin acid diterpenes displayed glutamic acid decarboxylase (GAD) inhibition. Inhibitors of these enzymes may have impacts on the control of reproduction since MAO metabolizes dopamine, an inhibitor of the neuroendocrine reproductive axis, while GAD synthesizes -aminobutyric acid (GABA), a stimulator of this axis. Bioassay-guided fractionations of effluents and wood feedstocks identified that medium polar extracts of primary- and secondary-treated effluents and balsam fir feedstock contained high GAD inhibitory activity. This activity was associated with chemically complex fractions rather than single active principles. Advanced metabolomic comparison of medium polar extracts of feedstock and treated effluent identified 15 common plant metabolites, demonstrating that phytochemicals entering the mill in wood are surviving pulp production and effluent treatment processes and may be responsible for observed GAD inhibition. Discriminant metabolomics analysis identified 4-acetylpyridine, a novel compound to be described in effluents, as well as two other tentatively identified compounds, as chemical markers of GAD inhibitory effluent fractions. Five tentatively identified chemical markers and (+)-lariciresinol were found in inhibitory balsam fir feedstock fractions. Neuroendocrine pathways that control reproduction in fish, such as dopamine and GABA pathways, are also important drug targets for the treatment of neurological disorders in mammals; therefore these results also have implications for the development of natural health products from phytochemicals and tree extracts common to Canadian forests. By using an interdisciplinary approach (phytochemistry, neuroendocrinology, ecotoxicology), I was able to explore the various implications of my research on the fields of natural health products chemistry and aquatic toxicology.
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COTELLESSA, LUDOVICA. "THE INVOLVEMENT OF THE NOTCH PATHWAY IN THE GNRH NEURONS DEVELOPMENT." Doctoral thesis, Università degli Studi di Milano, 2021. http://hdl.handle.net/2434/814079.
Full textAbstract:
The proper development of the hypothalamic-pituitary-gonadal (HPG) axis is essential for normal
reproductive competence. Misfunctions in the axis that impairs GnRH synthesis or function result in
GnRH deficiency. Idiopathic congenital hypogonadotropic hypogonadism (CHH) is a rare
reproductive disorder, with significant heterogeneity of genetic inheritance, that is primarily caused
by gonadotropin-releasing hormone (GnRH) deficiency. Clinically, the disorder is characterized by
an absence of puberty and infertility. In approximately 50% of cases, CHH patients also suffer from
a reduced or deficient sense of smell (hyposmia or anosmia, respectively). In this case, the disorder
is termed Kallmann syndrome (KS) and results from a failure or incomplete embryonic migration of
GnRH-producing neurons. The significance to elucidate the genetic causes of CHH is related to the
relatively high percentage (about 50%) of patients that are still considered idiopathic. It is known
from the literature that Notch signaling has a role in the migration of neurons in the developing cortex
and that it is expressed in the olfactory system of many species, so we would like to understand if
Notch signaling has a role in the migration of GnRH neurons in the olfactory system. Hence, the aim
of my PhD was to understand: 1) if Notch signaling molecules are expressed along the GnRH
migratory pathway in human fetal and adult post-mortem brain sections; 2) if Notch plays a role in
the establishment of the correct GnRH migratory process or GnRH axonal targeting to the
hypothalamic regions, using zebrafish as an in vivo model; 3) to address whether patients affected by
CHH present mutations in the Notch signaling pathway; 4) to functionally validate the eventual
mutations using an immortalized GnRH cell line (GN11).
We explored by multiplex fluorescent in situ hybridization and immunohistochemical assays the
expression of both JAG1, NOTCH1 and NOTCH2 in coronal human fetal sections of the nasal
compartment and nasal/forebrain junctions in early developmental stages. These experiments
revealed that JAG1, NOTCH1 and NOTCH2 are expressed along the GnRH migratory pathway during
human fetal development, suggesting a paracrine and/or autocrine mechanism. We then used
zebrafish as in vivo model to investigate the involvement of jag1 in GnRH3 neurons development
and migration. Firstly, we have demonstrated the expression of jag1a, jag1b, notch1a and GnRH3 in
the olfactory placode of zebrafish embryos, revealing a possible collaboration between these factors
in the GnRH3 neurons development. Taking advantage of the zebrafish transgenic line
tg(GnRH3:EGFP), we demonstrated that downregulation of jag1b, but not jag1a, strongly affects the
development of the GnRH3 neurons at 48 and 72hpf. Treatment of tg(GnRH3:EGFP) embryos with
the Notch inhibitor, DAPT (γ-secretase inhibitor), phenocopied the morpholino experiments, further
supporting a role for notch1/jag1 in the development of GnRH3 neurons. Additionally, we performed
migration assay on immortalized GnRH cells, and we observe that JAG1 act as a repellent factor for
the motility of these cells.
Based on the human and zebrafish data and considering the KS-like phenotype of our jag1b
morphants, we next sought in our cohort of CHH/KS patients for possible mutation in JAG1 gene and
four rare missense variants in the JAG1 gene were identified (R117G, F206Y, Y931I, 1160N).
Overexpression of all JAG1 variants in GN11 cell line coupled with an immunofluorescence assay
revealed that only the JAG1 variant D1160N was mislocalized and retained into the cytoplasm. The
functionality was evaluated through the Luciferase assay, and D1160N variant did not activate the
transcription of the Notch Responsive Element promoter. Combining morphological analysis in vivo
(in human and zebrafish), together with genetic and pharmacological manipulation in zebrafish, and
human genetic analysis, we provide compelling evidence that Notch1/Jag1 signaling has a role in the
development of GnRH neurons/olfactory system and indicate that Notch1/Jag1 signaling
insufficiency may contribute to the pathogenesis of CHH in humans.
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McClure-Sharp, Jilliane Mary, and mikewood@deakin edu au. "Regulation of corticotropin-releasing factor concentration and overflow in the rat central nervous system." Deakin University. School of Biological and Chemical Sciences, 1998. http://tux.lib.deakin.edu.au./adt-VDU/public/adt-VDU20060802.143911.
Full textAbstract:
Corticotropin-releasing factor (CRF) is the primary hormone of the hypothalamo-pituitary adrenal axis (HPA-axis). In addition to its endocrine function, it has been proposed that CRF acts as a neurotransmitter. The widespread distribution of CRF immunoreactivity and CRF receptors in the rat central nervous system (CNS) supports this theory. Immunohistochemical studies have demonstrated high levels of CRF immunoreactivity the rat hypothalamus, a brain region involved in the regulation and integration of a variety of endocrine and autonomic homeostatic mechanisms. CRF has been shown to be involved in a number of these activities such as blood pressure control, food and water intake, behaviour and emotional integration. Many of these activities demonstrate progressive dysfunction as ageing proceeds. The aim of this thesis was to investigate the regulation of CRF in the rat CNS, particularly over the period of maturation and ageing. Tissue extraction and peptide radioimmunoassay (RIA) techniques were developed in order to measure regional CRF concentrations as a function of age in the rat CNS. Seven brain regions were examined including the hypothalamus, pituitary, medulla oblongata, pons, cerebral cortex, cerebellum and midbrain. Three age ranges were investigated: 3 4 weeks, 4 5 months and 14 18 months, representing young, mature and old age groups. Data for the tissues of individual rats from each age group were analysed using one-way analysis of variance (ANOVA) with post-hoc Scheffé tests (SPSS Release 6 for Windows, 1989 1993). CRF were detected in measurable quantities in all brain regions examined. Different age-related patterns of change were observed in each brain region. CRF concentrations (ng/g tissue) were highest in the pituitaries of young rats and were significantly reduced over the period of maturation (P< 0.05). However, the high CRF concentration of the young rat pituitary was likely to be a factor of the smaller tissue mass. Although the absolute CRF content (ng/tissue) of this tissue appeared to decline with maturation and ageing, the reduction was not significant (P>0.05). Therefore the pituitary of the young rat was relatively enriched with CRF per gram tissue. The highest CRF concentration in mature and aged rats was measured in the hypothalamus, in accordance with previous immunohistochemical studies. Hypothalamic CRF concentrations (ng/g tissue) demonstrated no significant alterations with maturation and ageing. The absolute CRF content (ng/tissue) of the hypothalamus was significantly less in the young rat compared to mature and aged animals, however this was accompanied by a smaller tissue mass (P<0.05). The CRF concentrations (ng/g tissue) of the rat cerebral cortex and medulla oblongata demonstrated significant reduction with advancing age (P<0.05), however in both cases this appeared to be due to significant increases in mean tissue mass. The absolute CRF content of these tissues (ng/tissue) were not significantly different over the period of maturation and ageing (P>0.05). CRF concentration (ng/g tissue) and absolute content (ng/tissue) of the pons demonstrated a trend to increase with advanced age in the rat, however this was not significant in both cases (P>0.05). Of interest were the significant increases observed in the CRF concentrations of the cerebellum and midbrain (ng/g tissue with advanced ageing (P<0.05). Significant increases were also observed in the mean tissue mass and absolute CRF content (ng/tissue) of these regions in aged rats (P<0.05). These findings perhaps indicate increased CRF synthesis and or decreased CRF turnover in these tissues with advancing age. The second stage of these studies examined age-related alterations in basal and potassium-stimulated hypothalamic CRF and overflow over the period of maturation and ageing in the rat, and required the preliminary development of an in vitro tissue superfusion system. The concomitant release of the co-modulatory compound, neuropeptide Y (NPY) was also measured. NPY has been shown to positively regulate CRF release and gene expression in the hypothalamus. In addition, NPY has been demonstrated to be involved in a number of hypothalamic activities, including blood pressure control and food intake regulation. Hypothalamic superfusion data were analysed using one factor repeated measures ANOVA (SPSS Release 6 for Windows, 1989-1993) followed by least significant difference tests ( Snedecor and Cochran, 1967) to enable both time and age comparisons. Basal hypothalamic CRF overflow was unaltered with maturation and ageing in the rat. Potassium stimulation (56 mM) elicted a significant 2 3 fold increase in hypothalamic CRF overflow across age groups (P<0.05). Stimulated hypothalamic CRF overflow was significantly greater in the young rat compared to the mature and aged animals (P<0.05). The enhanced response to depolarizing stimulus was observed at an age when the absolute CRF content of the hypothalamus was significantly less that of other age groups. It is possible that the enhanced responsiveness of the young rat may be of survival advantage in life threatening situations. Basal hypothalamic NPY overflow was much less than that of CRF, and potassium stimulation resulted in a very different age-related profile. The hypothalamic NPY response to depolarization was significantly reduced in the young rat and declined significantly with advanced ageing (P<0.05). The contrasting profiles of stimulated CRF and NPY overflow may indicate the activity of alternative regulatory factors present in the hypothalamus, whose activity may also be affected in an age-related manner. The final stage of these studies examined the nature of NPY modulation of hypothalamic CRF overflow in the mature rat. The facilitatory effect of NPY on hypothalamic CRF overflow was confirmed. The application of NPY (0.1 µM) significantly increased CRF overflow approximately 4 fold of basal (P<0.05). In addition, the role of the NPY-Y1 receptor was investigated by the prior application of Y1 receptor antagonists, GW1229 (0.05 µM). At this concentration GW1229 significantly reduced hypothalamic CRF overflow induced by perfusion with NPY (0.1 µm), P<0.05. It was concluded the Y1 receptor does have a role in the regulation of hypothalamic CRF overflow by NPY.
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Halpern, Bruno. "O papel da melatonina na regulação do tecido adiposo marrom." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-31102018-131724/.
Full textAbstract:
O tecido adiposo marrom (TAM), caracterizado pela presença da proteína termogênica UCP-1, é conhecido há muitas décadas como um tecido termogênico em mamíferos, porém sua significância clínica em humanos era considerada pequena, com exceção de neonatos, até que o desenvolvimento e uso de métodos de PET-FDG terem demonstrado que humanos adultos também possuem TAM ativo, especialmente após exposição ao frio. Essa descoberta levou a um enorme aumento nas pesquisas sobre o assunto, já que sua ativação, levando a um aumento do gasto energético, poderia, pelo menos na teoria, ser uma possível arma no tratamento da obesidade e diabetes tipo 2 e sua redução ou ausência ser uma causa de ganho de peso. Muitos compostos vêm sendo estudados como possíveis recrutadores e ativdadores desse tecido. A melatonina é um deles, embora nenhum estudo tenha sido feito em humanos. A melatonina, um hormônio pineal sintetizado à noite com um papel crítico na sincronização do ritmo circadiano, é estudado há várias décadas como um regulador chave do metabolismo energético em diversas espécies animais. Ratos pinealectomizados ganham peso e tem distúrbios metabólicos durante sua vida, e a suplementação noturna de melatonina, reverte estas alterações, sem redução da ingesta alimentar. Devido a isso, uma hipótese é que o papel central da melatonina no metabolismo energético inclui sua função no gasto energético, possivelmente relacionado à ativação do TAM. Muitos modelos experimentais, a maioria em animais hibernantes, demonstraram o papel da melatonina no recrutamento do TAM. Nesse estudo, o objetivo é determinar se a suplementação de melatonina para indivíduos e animais de experimentação (ratos Wistar) deficientes de melatonina aumenta sua ativação. Foi encontrado que, em ratos Wistar, animais pinelaectomizados possuem uma capacidade termogênica do TAM reduzida após exposição ao frio comparado com a temperatura ambiente, e a suplementação de melatonina normaliza essa capacidade termogênica. Esse dado sugere um papel da melatonina na resposta máxima de ativação do TAM após um desafio ao frio agudo. Também foi observado um aumento de expressão de UCP-1 (RNA) em animais repostos com melatonina, tanto em controles como em pinealectomizados, e animais pinealectomizados não repostos apresentam uma expressão de UCP-1 menor que um grupo controle. Em humanos, a suplementação de melatonina aumenta o volume e atividade do TAM em quatro indivíduos pinealectomizados (por tumores pineais) com baixo nível de melatonina no basal, analisado por tomografia de emissão de prótons acoplada a ressonância magnética (PET-RM). Embora a análise do TAM em ambos os protocolos tenha sido distinta, seus resultados apontam para a mesma regulação positiva do TAM pela melatonina. A termografia infravermelha (TIV) foi também realizada em humanos, com aumento de atividade de TAM após exposição ao frio, poréma correlação entre as respostas com a TIV e o PET-RM foi moderada e não significativa. Diferenças entre o protocolo frio e limitação da TIV em indivíduos mais obesos podem ter contribuído para esses resultados. Uma relação positiva da suplementação de melatonina nos lípides (principalmente colesterol e triglicérides) também foi encontrada, porém sem impacto na gordura hepáticaBrown adipose tissue (BAT), characterized by the presence of the thermogenic protein UCP-1 have long been known as a thermogenic tissue in mammals, however its significance in humans was considered minor, with the exception of newborns, until FDG-PET exams demonstrated that human adults still have active BAT, especially after cold exposure. This prompted to an incredible increase in research on the field, since its activation, leading to increased energy expenditure could, at least theoretically, be a possible tool for the treatment of obesity and type 2 diabetes and its reduction or absence be a cause of weight gain. Many compounds aiming to recruit and activate BAT have been studied. Melatonin has been one of them, although no study has been performed in humans. Melatonin, a pineal hormone synthetized at night with a critical role in the synchronization of circadian rhythms, has long been studied as a key regulator of energy metabolism in many animal species. Pinealectomized rats gain weight and have metabolic disturbances during life, and the circadian supplementation of melatonin, at night, reverts these alterations, without decrease in energy intake. Due to that, it is hypothesized that a main role of melatonin in energy metabolism includes its action on energy expenditure, possibly related to activation of BAT. Many experimental models, mainly in hibernating animals, have shown a role of melatonin on BAT recruitment. In the present study, we ought to determine if the supplementation of melatonin for melatonin deficient subjects and experimental animals (Wistar rats) increases BAT activation. We found, in Wistar rats, that pinealectomized animals have a reduced BAT thermogenic capacity after acute cold exposure compared with ambient temperature, and melatonin supplementation in this animals leads to normalization of BAT thermogenic capacity. This data suggests a role of melatonin in improving the maximal response of BAT after an acute challenge. We also found that melatonin supplementation increases UCP-1 RNA expression both in control and pinealectomized rats, and pinealectomized rats without supplementation have a reduced UCP-1 expression compared with controls. In humans, we found that melatonin supplementation increased BAT volume and activity in four pinealectomized (due to pineal tumors) individuals with low melatonin at baseline, analyzed by Positron Emission Tomography associated with magnetic resonance (PET-MR). Although the analysis of BAT in both studies was different, their results point to the same positive regulation of BAT by melatonin. We also performed infrared termography (IRT) in humans, but the results were not conclusive since although we also found an increase in BAT activity measured in Watts, the correlation between the methods was moderate. The difference may be due to different protocols of cold exposure between methods, probably inadequate in IRT, as well as maybe to a limitation of IRT in more obese individuals. We also found that melatonin supplementation in melatonin deficient humans may have a positive impact on blood lipid concentrations, (mainly total cholesterol and triglycerides) but, at least for the time studied, does not appear to have an impact on liver fat
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Kaye, Joey Michael. "Mechanisms and clinical implications of the neuroendocrine response to a novel carbon dioxide stressor in man." University of Western Australia. School of Medicine and Pharmacology, 2005. http://theses.library.uwa.edu.au/adt-WU2005.0099.
Full textAbstract:
Maintenance of normal health requires an intact stress system capable of mounting the metabolic, autonomic, behavioural and motor responses required for coping with or avoiding physiological and pathological challenges. The neuroendocrine component of this response principally involves the hypothalamic-pituitary-adrenal (HPA) and sympatho-adrenomedullary (SAM) axes. Impaired regulation of these axes has been implicated in the pathogenesis and expression of numerous disease states, however, it has proved very difficult to reproducibly activate the HPA and SAM axes and no single test exists that can reliably and safely be used to study these systems in man. Carbon dioxide (CO2) is the principal regulator of respiration, acid-base balance and behavioural-state arousal in humans. Paradigms of CO2 inhalation have been used in psychiatric research to investigate panic and anxiety disorders, but evaluation of other components of the stress response to CO2 has not previously been performed. I hypothesised that a single breath of 35% CO2 would be a simple and reliable tool for the evaluation of the stress response in humans. A single breath of four doses of CO2 (5%, 25%, 35% and 50%) was administered to 9 healthy volunteers in a randomised, single blind fashion. Subjective symptoms of anxiety increased in a dose-dependent manner. Inhalation of a single breath of 35% CO2 stimulated significant ACTH (p = 0.006), noradrenaline (p < 0.0001), cortisol (p = 0.02) and prolactin (p = 0.002) release. It also provoked an acute pressor response and an associated bradycardia (p < 0.0001 for both). No significant habituation of psychological, HPA or cardiovascular responses was seen when this dose was repeated after one week (n = 10) or 6 months (n = 5). It was apparent that a single breath of 35% CO2 reliably and safely produced SAM and HPA axis activation and further studies were then undertaken to assess the mechanism by which the observed responses occurred and its potential clinical implications. Administration of naltrexone (an opiate antagonist) to 10 normal volunteers disinhibited the HPA axis (p < 0.0004), whilst administration of metyrapone (a cortisol synthesis inhibitor) significantly reduced baseline cortisol (p < 0.03) levels. However, this alteration in HPA axis activity had no effect on either cardiovascular or psychological responses. Further, in a study of 8 breastfeeding mothers (a state associated with physiological suppression of the HPA axis) suckling significantly reduced plasma cortisol levels compared with control (p = 0.002) and bottle-feeders (p = 0.003). Despite this cortisol, systolic blood pressure (SBP), heart rate and psychological responses to 35% CO2 were not affected
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Anderson, Greg Muir. "Role of thyroid hormones in the neuroendocrine control of seasonal reproduction in red deer hinds." Lincoln University, 1997. http://hdl.handle.net/10182/2139.
Full textAbstract:
A series of eight experiments was conducted to investigate the requirement for thyroid hormones in neuroendocrine processes which lead to the seasonally anoestrous state in red deer hinds. The first two experiments used thyroidectomized, ovariectomized, oestradiol-treated hinds which received various thyroid hormone replacement treatments (n=5 per group) to investigate the timing and dose-responsiveness of thyroid hormones in bringing about seasonal oestradiol-induced suppression of plasma LH concentration. A significant seasonal decline in mean plasma LH concentration during September (coinciding with the onset of anoestrus in entire cycling hinds in New Zealand) was observed in all thyroidectomized hinds in both experiments regardless of T₄ or T₃ treatment. When oestradiol implants were removed in November or December, mean plasma LH concentrations increased significantly in all but one of hinds in which T₄ had been administered at very low doses by subcutaneous implants, and mean plasma LH concentrations and LH pulse amplitude increased in approximately half of hinds administered T₃ at varying doses by subcutaneous injections over a one-week period in October. These results suggested that thyroid hormones are not required for steroid-dependent reproductive suppression, but could possibly play a role in steroid-independent suppression of LH secretion. Because problems were encountered in delivering appropriate doses of thyroid hormones in both experiments, further confirmation of these findings was required. Therefore in the next experiment the role of thyroid gland secretions was examined in euthyroid (n=5) and thyroidectomized (n=4) ovariectomized hinds treated with oestradiol implants. These implants were removed for about one month on three occasions to examine the effect of thyroidectomy on steroid-independent control of seasonal LH secretion. During the non-breeding season basal and GnRH-induced plasma LH concentrations declined in all hinds in the presence of oestradiol, but returned to breeding season levels when oestradiol was withdrawn in November. In a concurrent experiment, thyroidectomy of ovary-entire hinds (n=7) during the breeding season prevented the cessation of oestrous cyclicity in spring; this was in contrast to oestrous cyclicity in T₄replaced (n=4) or euthyroid control (n=5) hinds which ceased to occur in early September. Collectively, these results indicate that thyroid hormones are required for the termination of the breeding season in cycling red deer hinds and that this action occurs via steroid-independent neuroendocrine pathways. Two experiments were conducted using neurotransmitter receptor agonists and antagonists to identify neural pathways in the brain which mediate LH suppression by oestradiol and by steroid-independent mechanisms, and to test if the thyroid gland is required for activation of these pathways during the non-breeding season. It was concluded from the lack of plasma LH responses to dopaminergic and opioidergic agonists and antagonists in ovariectomized and ovariectomized, thyroidectomized hinds (n=5) that neural pathways involving dopamine-D₂receptors do not mediate oestradiol-induced seasonal suppression of plasma LH concentrations, and neither dopaminergic or opioid neural pathways mediate non-steroidal suppression of plasma LH concentrations. However preliminary evidence was obtained for a stimulatory role of serotonergic neural pathways in controlling LH secretion. Another experiment was conducted to identify when the steroid-independent mechanisms which suppress LH concentrations during the non-breeding season are responsive to thyroid hormones. T₄treatment at the beginning of or during the non breeding season was effective in bringing about suppression of plasma LH concentration in thyroidectomized, ovariectomized hinds (n=5 per group), but this action of thyroid hormones did not occur during the breeding season. These results show that the steroid-independent mechanisms which contribute to seasonal suppression of plasma gonadotrophin concentrations require thyroid hormones to be present only from around the time of the end of the breeding season for their normal expression, and they remain responsive to thyroid hormones after this period. Lastly, the feasibility of achieving out-of-season breeding using thyroidectomized hinds (n=9) was evaluated by comparing oestrous behaviour, ovulation and pregnancy rates to those of euthyroid control hinds (n=7) following synchronization of oestrous cycles. There was a non-significant trend for a greater occurrence of oestrous behaviour and ovulation in thyroidectomized hinds compared with euthyroid controls during the non-breeding season, but the pregnancy rate following out-of season mating with a thyroidectomized stag was low, suggesting that a side effect of thyroidectomy may be impaired fertility. Six out-of-season pregnancies were obtained from eight matings, however because three of these pregnancies occurred in euthyroid control hinds no improvement in out-of-season reproductive performance could be attributed to thyroidectomy. It is likely that if the actions of the thyroid glands are to be exploited as a tool for achieving out-of-season breeding in this species, techniques will have to be developed for specifically blocking or overcoming the effects of thyroid hormones on the reproductive neuroendocrine centres without causing general hypothyroidism and its associated side-effects.
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Emmerson, Michael George. "Adolescent stress and social experiences : developmental antecedents of adult behavioural responses to unfamiliar stimuli and the underlying neuroendocrine mechanisms." Thesis, University of St Andrews, 2017. http://hdl.handle.net/10023/12094.
Full textAbstract:
During adolescence, animals leave the natal home and interact with potentially threatening stimuli (i.e. stressors), e.g. unfamiliar environments and conspecifics. Adolescent stressors can result in fewer interactions with unfamiliar stimuli in adulthood, plausibly due to sustained effects of glucocorticoid exposure on stress physiology (e.g. glucocorticoid secretion and receptor expression). The current thesis tested the hypothesis that adolescent glucocorticoid exposure and social experiences act as stressors by quantifying the effects of the adolescent experiences on behavioural responses to unfamiliar stimuli and the underlying neuroendocrine mechanisms when in adulthood using two captive species, zebra finches and rats. In study one, adolescent zebra finches were dosed with the glucocorticoid corticosterone. In adulthood, birds dosed with corticosterone in early adolescence took longer to enter an unfamiliar environment when tested individually and had lower expression of the glucocorticoid receptor GR in the hippocampus and hypothalamus, brain regions that regulate stress responses. Glucocorticoids therefore appear to be an endocrine mechanism behind the long-term effects of adolescent stress. Subsequent studies explored whether higher social density and more unfamiliar social interactions during adolescence act as stressors. In study two, early adolescent zebra finches were housed in groups varying in conspecific number and density. In adulthood, females raised in larger groups secreted a higher stressor-induced corticosterone concentration and, if raised at lower density, spent more time in an unfamiliar environment when group housed. In study three, adolescent female rats were housed in familiar pairs or exposed to unfamiliar conspecifics. Unfamiliar adolescent interactions had no effects on responses to unfamiliar environments or stress physiology in adulthood, but heightened ultrasonic call rates. In this thesis, adolescent social experiences do not act like stressors, but modulate (especially female) social behaviour. Adolescent stressors and social experiences therefore have distinct effects on responses to unfamiliar stimuli and stress physiology that are maintained into adulthood.