Prenatal ethanol (E) exposure has marked effects on development of the hypothalamic-pituitary-adrenal (HPA) and -gonadal (HPG) axes. E rats show HPA hyperresponsiveness to stressors and altered reproductive function in adulthood. Importantly, prenatal ethanol differentially alters stress responsiveness in adult males and females, raising the possibility that gonadal hormones play a role in mediating ethanol effects on HPA function. To address this possibility, two studies were conducted to test the hypothesis that the differential alterations in HPA activity observed in E compared to control males are mediated, at least in part, by ethanol-induced changes in HPG effects on HPA regulation. The first study compared the effects of gonadectomy (GDX) on HPA and HPG activity in adult male offspring from prenatal E, pair-fed (PF) and ad libitum-fed control (C) dams. There were no differences among groups in basal testosterone levels under intact conditions. However, E males showed increased adrenocorticotropin but blunted testosterone and luteinizing hormone (LH) responses to restraint stress compared to PF and/or C rats, and no stress-induced elevation in arginine vasopressin (AVP) mRNA levels. GDX eliminated these differences among groups. The second study explored dose-related effects of testosterone on HPA regulation. Testosterone had less of an inhibitory effect on stress-induced CORT and LH increases in E than in PF and C males. Furthermore, testosterone had a reduced effect on central corticotropin-releasing hormone pathways, but an increased effect on central AVP pathways in E compared to PF and/or C males. Importantly, reduced androgen receptor (AR) mRNA levels, possibly reflecting downregulation of AR in key brain areas, may counteract the increased inhibitory AVP signals upstream from the paraventricular nucleus, and thus contribute to the HPA hyperresponsiveness seen in E males. Together these findings suggest that central regulation of both the HPA and HPG axes are altered by prenatal ethanol exposure. The capacity of testosterone to regulate HPA activity is altered in E males, with some effects mediated by the nutritional effects of ethanol. These changes would impair the ability to maintain homeostasis in E animals and have implications for the development of secondary disabilities in children with Fetal Alcohol Spectrum Disorder.

Prenatal ethanol (E) exposure has marked effects on development of the hypothalamic-pituitary-adrenal (HPA) and -gonadal (HPG) axes. E rats show HPA hyperresponsiveness to stressors and altered reproductive function in adulthood. Importantly, prenatal ethanol differentially alters stress responsiveness in adult males and females, raising the possibility that gonadal hormones play a role in mediating ethanol effects on HPA function. To address this possibility, two studies were conducted to test the hypothesis that the differential alterations in HPA activity observed in E compared to control males are mediated, at least in part, by ethanol-induced changes in HPG effects on HPA regulation. The first study compared the effects of gonadectomy (GDX) on HPA and HPG activity in adult male offspring from prenatal E, pair-fed (PF) and ad libitum-fed control (C) dams. There were no differences among groups in basal testosterone levels under intact conditions. However, E males showed increased adrenocorticotropin but blunted testosterone and luteinizing hormone (LH) responses to restraint stress compared to PF and/or C rats, and no stress-induced elevation in arginine vasopressin (AVP) mRNA levels. GDX eliminated these differences among groups. The second study explored dose-related effects of testosterone on HPA regulation. Testosterone had less of an inhibitory effect on stress-induced CORT and LH increases in E than in PF and C males. Furthermore, testosterone had a reduced effect on central corticotropin-releasing hormone pathways, but an increased effect on central AVP pathways in E compared to PF and/or C males. Importantly, reduced androgen receptor (AR) mRNA levels, possibly reflecting downregulation of AR in key brain areas, may counteract the increased inhibitory AVP signals upstream from the paraventricular nucleus, and thus contribute to the HPA hyperresponsiveness seen in E males. Together these findings suggest that central regulation of both the HPA and HPG axes are altered by prenatal ethanol exposure. The capacity of testosterone to regulate HPA activity is altered in E males, with some effects mediated by the nutritional effects of ethanol. These changes would impair the ability to maintain homeostasis in E animals and have implications for the development of secondary disabilities in children with Fetal Alcohol Spectrum Disorder.

Prenatal ethanol (E) exposure has marked effects on development of the hypothalamic-pituitary-adrenal (HPA) and -gonadal (HPG) axes. E rats show HPA hyperresponsiveness to stressors and altered reproductive function in adulthood. Importantly, prenatal ethanol differentially alters stress responsiveness in adult males and females, raising the possibility that gonadal hormones play a role in mediating ethanol effects on HPA function. To address this possibility, two studies were conducted to test the hypothesis that the differential alterations in HPA activity observed in E compared to control males are mediated, at least in part, by ethanol-induced changes in HPG effects on HPA regulation. The first study compared the effects of gonadectomy (GDX) on HPA and HPG activity in adult male offspring from prenatal E, pair-fed (PF) and ad libitum-fed control (C) dams. There were no differences among groups in basal testosterone levels under intact conditions. However, E males showed increased adrenocorticotropin but blunted testosterone and luteinizing hormone (LH) responses to restraint stress compared to PF and/or C rats, and no stress-induced elevation in arginine vasopressin (AVP) mRNA levels. GDX eliminated these differences among groups. The second study explored dose-related effects of testosterone on HPA regulation. Testosterone had less of an inhibitory effect on stress-induced CORT and LH increases in E than in PF and C males. Furthermore, testosterone had a reduced effect on central corticotropin-releasing hormone pathways, but an increased effect on central AVP pathways in E compared to PF and/or C males. Importantly, reduced androgen receptor (AR) mRNA levels, possibly reflecting downregulation of AR in key brain areas, may counteract the increased inhibitory AVP signals upstream from the paraventricular nucleus, and thus contribute to the HPA hyperresponsiveness seen in E males. Together these findings suggest that central regulation of both the HPA and HPG axes are altered by prenatal ethanol exposure. The capacity of testosterone to regulate HPA activity is altered in E males, with some effects mediated by the nutritional effects of ethanol. These changes would impair the ability to maintain homeostasis in E animals and have implications for the development of secondary disabilities in children with Fetal Alcohol Spectrum Disorder. / Medicine, Faculty of / Graduate

Les écosystèmes marins constituent une cible majeure des changements globaux qui affectent de façon pérenne notre planète.Nous nous sommes intéressés à deux de ces changements susceptibles de menacer le milieu marin : le réchauffement climatique par le biais de l’étude de l’effet du stress thermique sur l’expression de ho-1 et la pollution via l’étude de l’impact des métaux lourds à effets perturbateurs endocriniens (le cadmium et le plomb) sur l’axe hypothalamo-hypophyso-gonado-hépatique (HHGH) chez le loup (Dicentrarchus labrax L.).Nos résultats montrent une réponse importante de ho-1 aux stress thermique et chimique dans le foie. Nous avons également démontré une forte accumulation hépatique du Cd, et à un degré moindre du Pb, accompagnée d’une sur-expression du gène mt codant pour les métallothionéines. Des variations dans l’expression de gènes clés le long de l’axe HHGH (arom b, fshß, arom a…) ont été observées après intoxication par les deux métaux sans pour autant induire des effets physiologiques observables.La question se pose de savoir si la synergie des stress physico-chimiques impacte la dynamique et l’état sanitaire des populations marines. / Marine ecosystems are a major target of global changes that continuously affect our planet. In the present study we investigated two of these changes that may threaten the marine environment: global warming, through the study of the effect of heat stress on ho-1 expression and marine pollution through the study of the impact of heavy metals acting as endocrine disruptors (cadmium and lead) on the hypothalamic-pituitary-gonadal-liver (HHGL) axis in the sea bass (Dicentrarchus labrax L.). Our results show an important response of ho-1 to both thermal and chemical stress in the liver. We also demonstrated a high hepatic accumulation of Cd, and to a lesser extent of Pb. This accumulation was correlated with an overexpression of mt gene coding for metallothionein. Changes in the expression of candidate genes (arom b, fshß, arom a…) along the HHGL axis were observed after metal intoxication but no physiological effects were observed.The question then arises to what extent the synergy of physicochemical stressors impacts the dynamics and the welfare of marine species.

Thesis (Ph. D.)--Michigan State University. Dept. of Zoology & Environmental Toxicology, 2008. / Title from PDF t.p. (viewed on Mar. 30, 2009) Includes bibliographical references. Also issued in print.

京都大学 / 0048 / 新制・課程博士 / 博士(医学) / 甲第20613号 / 医博第4262号 / 新制||医||1023(附属図書館) / 京都大学大学院医学研究科医学専攻 / (主査)教授 小川 修, 教授 篠原 隆司, 教授 近藤 玄 / 学位規則第4条第1項該当 / Doctor of Medical Science / Kyoto University / DFAM

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Charles University in Prague Faculty of Pharmacy in Hradec Králové Department of Biological and Medical Science Author: Marcela Čuchalová Supervisor: doc. MUDr. Josef Herink, DrSc. Title of diploma thesis: The hypothalamic - pituitary - gonadal axis and epilepsy: mutual relationships The content of the diploma thesis is an overview of the anatomy and physiology of the hypothalamic-pituitary-gonadal axis (HHG). Further chapters are devoted to the influence of epilepsy on HHG function, the effect of HHG hormones on epileptic activity itself. The effect of anti-epileptics on HHG functions will also be elucidated. The second part of the diploma thesis deals with separate chapters - catamenial epilepsy and epilepsy during pregnancy. Keywords: antiepileptic drugs, gonadotropin, hypothalamic-pituitary-gonadal axis, prolactin, sex hormones, temporal lobe epilepsy.

No description available.

Le RFRP est une neuropeptide impliqué dans la régulation de l’axe reproducteur, mais ses effets varient en fonction du sexe et des espèces. Le but de cette étude était de décrire en détails l’organisation du système RFRP et de caractériser son rôle dans le contrôle circadien et saisonnier de l’axe reproducteur de hamsters femelles. Les résultats montrent que le système RFRP est régulé par la photopériode et que son niveau d’expression est plus élevé chez les femelles que chez les mâles. Cela se traduit par des actions spécifiques sur l’axe gonadotrope femelle. En effet, L’activité des neurones à RFRP est diminuée au moment du pic pré-ovulatoire de LH et des injections centrales de RFRP-3 dans l’heure qui précède le pic de LH induisent une diminution de l’amplitude de la sécrétion de LH, démontrant une implication du RFRP dans la régulation circadienne du pic pré-ovulatoire de LH. Par ailleurs, des infusions chroniques de RFRP-3 chez des hamsters femelles sexuellement inactifs sont capables de réactiver le fonctionnement de l‘axe reproducteur, ce qui montre que le RFRP a un également un rôle régulateur essentiel dans le contrôle saisonnier de la reproduction. / RFRP neurons regulate the reproductive axis, however, their effects depend on species and sex. Here, we aimed at providing a neuroanatomical description of the RFRP system in the Syrian hamster and at investigating the role of RFRP in the daily and seasonal control of female reproduction. We show that besides being regulated by annual changes in photoperiod, the RFRP system is more strongly expressed in females than in males. In line with this, we unveil that RFRP has multiple roles in regulating female reproduction. RFRP neuronal activity is specifically reduced at the time of the pre-ovulatory LH surge and central RFRP-3 administration prior to the surge decreases LH peak levels, altogether pointing towards a daily down-regulation of the inhibitory RFRP signal necessary for proper generation of the LH surge. Moreover, chronic RFRP-3 infusion in sexually inactive females, with endogenous low RFRP expression, completely reactivates the reproductive axis. Taken together, we demonstrate that RFRP is a key component in the seasonal control of reproduction while at the same time specifically regulating cyclic events controlling reproductive activity in females.