Thesis (doctoral)--Ludwig Maximilians-Universität zu München, 1979.

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / "May 2000." Typescript. Vita. Includes bibliographical references (leaves 166-187). Also available on the Internet.

Thesis (doctoral)--University of Geneva, 1979. / "Thèse No. 3753." Includes bibliographical references (p. 17-19).

Orientador: Rita Cássia Menegati Dornelles / Coorientadora: Maristela de Oliveira Poletini / Banca: Cristina Mota Leite / Banca: Grace Schenatto Pereira Moraes / Banca: Luciana Pinato / Banca: Rovena Clara Galvão Januário Engelberth / Resumo: O envelhecimento é considerado processo multidimensional no qual fatores ambientais podem proteger ou, inversamente, agravar seus sinais, de maneira não linear, nos processos fisiológicos e neurocomportamentais. Durante este processo, os ritmos circadianos são interrompidos ou fragmentados com dissociação consequente dos ritmos circadianos do indivíduo e disfunções relacionadas ao relógio circadiano contribuem para o envelhecimento e para patologias a ele relacionadas. O objetivo deste estudo foi averiguar possível alteração temporal do sistema CLOCK no eixo HPG e a relação com às alterações hormonais que caracterizam a periestropausa. Foram utilizadas fêmeas adultas com ciclo estral regular (CD) na fase do diestro e fêmeas senis com ciclo estral irregular e persistência da fase do diestro (IDP). Para análises de expressão gênica dos clock genes Per2, Rev-erbα e Bmal1 no eixo HPG, foram utilizados punchs das regiões do NSQ, onde também foi analisado RNAm de AVP, APO e HMB destes animais, além da adenohipófise e ovários dos quais se extraiu o RNA para confecção do cDNA e realização de qPCR. A determinação da atividade neuronal vasopressinérgica no NSQ foi realizada por imunoistoquíca com dupla marcação para cFos e AVP em tecido previamente fixado com paraformaldeído. A concentração plasmática de gonadotrofinas foi determinada por radioimunoensaio. De modo geral, os animais IDP revelaram alterações no perfil de expressão gênica durante o fotoperíodo, com redução de amplitude, d... (Resumo completo, clicar acesso eletrônico abaixo) / Abstract: Aging is considered a multidimensional process in which environmental factors can protect or, conversely, aggravate its signals, non-linearly, in physiological and neurobehavioral processes. During this process, circadian rhythms are disrupted or fragmented with consequent dissociation of the individual's circadian rhythms and circadian clock-related dysfunctions contribute to aging and related pathologies. The objective of this study was to investigate possible temporal alteration of the CLOCK system in the HPG axis and the relation with the hormonal changes that characterize periestropause. Adult females with regular estrus cycle in the diestrous phase (RD) and old females with irregular estrous cycle and persistent diestrous phase (IPD). For analyzes of the gene expression of the genes Per2, Rev-erbα and Bmal1 in the HPG axis, punchs from the NSQ regions were used, where AVP, POA and MBH RNAm from these animals were also analyzed, as well as the adenohypophysis and ovaries from which they were extracted the RNA for cDNA production and qPCR performance. The determination of the vasopressinergic neuronal activity in the NSQ was performed by immunohistochemical with double labeling for cFos/AVP in tissue previously fixed with paraformaldehyde. The plasma concentration of gonadotrophins was determined by radioimmunoassay. In general, the IPD animals show alterations in the gene expression profile during the period analyzed, with amplitude reduction, phase shift / misalignment and absence of antiphase. The NSQ of IPD animals presented lower expression of Rev-erbα and higher RNAm expression for AVP than RD group. The relative quantification of Bmal1 was similar in both groups and there were no differences between groups in the expression of Per2. In PAO, IPD animals showed higher expression of Per2 and less amount of RNAm for Rev-erbα. MBH showed lower expression for Per2 and Rev-erbα and higher... / Doutor

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / "August 2000." Typescript. Vita. Includes bibliographical references (leaves 189-210). Also available on the Internet.

Thesis (doctoral)--University of Utrecht, 1983. / Summary in English and Dutch. Includes bibliographical references.

Immunocytochemical studies have demonstrated that nerve fibers containing immunoreactive oxytocin and vasopressin project to many areas of the central nervous system, including the hippocampus and the lateral septum (Buijs, 1980; Sofroniew and Weindl, 1978). Biochemical, physiological and behavioral studies of the effects of these peptides on the CNS have indicated that they are involved in functions as diverse as the control of serotonin turnover (Auerbach and Lipton, 1982), the regulation of body temperature (Kasting et. al., 1979) and the retention of conditioned behavior (de Wied et. al., 1974; Koob and Bloom, 1982). The presence of immunoreactive vasopressin (iAVP) in the hippocampus of Wistar rats was confirmed by radioimmunoassay. The vasopressin content of the dorsal hippocampus was 30.3 ± 7.3 pg iAVP/mg soluble protein and that of the ventral hippocampus was 81.4 ± 8.3 pg iAVP/mg soluble protein, while tissue from the cerebral cortex contained no detectable vasopressin. That this immunoreactivity was due to vasopressin was confirmed by the absence of immunoreactivity in hippocampal or cortical tissue from Brattleboro rats, which are genetically unable to synthesize vasopressin. Vasopressin applied by iontophoresis was found to increase the activity of neurones in the lateral septum and in the hippocampus of the anesthetized rat. There was no obvious difference between the response of spontaneously active cells and the response of cells excited by continuous iontophoresis of glutamate or acetylcholine. Repeated application of vasopressin resulted in a decline in the magnitude of the response, but at least part of this decline was due to progressive blockage of the micropipette barrel rather than to tachyphylaxis. Oxytocin, tested only in the septum, was without effect. When applied by superfusion onto rat hippocampal slices, the NHP peptides were found to increase the activity of 88% of spontaneously active cells and to induce activity in many neurones that were not spontaneously active. Arginine vasopressin, lysine vasopressin, arginine vasotocin, and oxytocin were found to be of roughly equivalent potency, producing a dose dependent response in the range 10⁻⁹-10⁻⁶M. Most cells were tested with more than one peptide and were always found to respond either to all or to none of them. There was no decline in responsiveness when cells were subjected to repeated applications of peptide, but continuous application caused the cells to become unresponsive. Following continuous application of oxytocin, a cell failed to respond to both oxytocin and vasopressin, as would be expected if the two peptides were acting on the same receptor. The analogues ddOT, ddAVP, and Gly⁷0T were also active, but the oxytocin fragment PLG had no effect, and the vasopressin fragment DGAVP was extremely weak. The response to the peptides could be blocked by vasopressin antagonists. The peptide sensitive cells appeared to be pyramidal cells rather than interneurones, since the peptide induced activity could be inhibited for about 200-600 msec by electrical stimulation of the stratum radiatum. / Arts, Faculty of / Philosophy, Department of / Graduate

Vasopressin, a hormone released from the neurohypophysis, contributes to the regulation of body fluid balance through its known actions on the kidney and the vasculature. Release of vasopressin is influenced by plasma osmolality and by afferent activity from sensory receptors in the high and low pressure vascular systems. Previous studies have not defined the relative importance of the carotid sinus baroreceptors, aortic baroreceptors and atrial receptors in the control of the plasma concentration of vasopressin in the rabbit. Experiments were carried out in anaesthetized rabbits to define the quantitative relationship between stimulation of the carotid sinus baroreceptors and the plasma concentration of vasopressin. This relationship was examined in the presence and absence of afferent input from the aortic and atrial receptors. Changes in blood volume were induced to produce a change in the stimulus to the aortic baroreceptors and atrial receptors at high or low, constant carotid sinus pressure. Section, of the aortic depressor nerves and the vagus nerves allowed examination of the individual contributions of atrial receptors or aortic baroreceptors on the plasma concentration of vasopressin. It was also possible to examine the interaction between the carotid sinus baroreceptors and the aortic and atrial receptors. The results showed that plasma concentration of vasopressin was reduced by minimal stimulation of carotid sinus baroreceptors and that maximal inhibition of the release of vasopressin was achieved with a relatively low total arterial baroreceptor input. No influence of carotid sinus baroreceptors on vasopressin release was seen in the presence of intact aortic baroreceptors demonstrating the important interaction between the effects of stimulation of these two sets of receptors. It was not possible to demonstrate, in the rabbits used in this study, a significant contribution of atrial receptors to the control of vasopressin release either in response to changes in carotid sinus pressure or in response to changes in blood volume. To minimize the inhibitory effect of arterial baroreceptors on the release of vasopressin the aortic depressor nerves were cut and carotid sinus pressure was set at a low level. It was still not possible to demonstrate an effect of a reduction in blood volume on vasopressin release, confirming the absence of a contribution from atrial receptors in the anaesthetized rabbit. There appears to be considerable variation between species in the contribution of the different receptor groups to the release of vasopressin. The results suggest that in the normal rabbit there is likely to be significant tonic inhibition of the release of vasopressin by stimuli arising from arterial baroreceptors. The absence of a demonstrable influence of atrial receptors in these rabbits is consistent with findings in primates but differs from those in dogs. It is unlikely that changes in plasma vasopressin concentration induced by small changes in blood volume contribute to the control of arterial pressure through direct effects on vascular resistance and capacitance. / Medicine, Faculty of / Cellular and Physiological Sciences, Department of / Graduate

Thesis (Ph. D.)--University of Missouri--Columbia, 2000. / Typescript. Vita. Includes bibliographical references (leaves 166-187). Also available on the Internet.

Diversos estudos demonstram que o aumento da osmolaridade é capaz de causar simpatoexcitação e aumento da pressão arterial, estando o núcleo paraventricular do hipotálamo (PVN) envolvido em tal resposta. Evidências recentes demonstraram um papel da VP modulando a atividade de neurônios do PVN envolvidos com o controle da atividade simpática. Deste modo, o objetivo deste estudo foi investigar o papel da vasopressina, por meio de sua ação no PVN, sobre as alterações na atividade simpática em situações de hiperosmolaridade. Nossos resultados demonstraram que a VP microinjetada bilateralmente no PVN foi capaz de promover um aumento significativo NA ansl. O antagonismo bilateral dos receptores V1a no PVN em animais submetidos à sobrecarga de sal promoveu uma queda significativa na ANSL, a qual não foi observada em animais normohidratados. O conjunto dos resultados nos permite afirmar que a VP agindo diretamente em neurônios do PVN é capaz de alterar a atividade simpática, participando da resposta simpatoexcitatória observada durante aumento da osmolaridade. / Diverse studies demonstrated that osmorality increase is able of causing simpatoexcitação and increase in arterial pressure, with paraventricular hypothalamic nucleus (PVN) involved in this response. Studies showed an role of VP modulating the activity of neurons in the PVN involved in the control of sympathetic activity. In this way, the aim of this study was to investigate the role of the vasopressina, through it\'s action in the PVN, over the alterations in the sympathetic activity induced by hiperosmolality.The results showed that bilateral microinjection of VP into the PVN is able of increase significatively the lumbar sympathetic nerve activity. Moreover, the bilateral block of the V1a receptors into PVN of animals subjected to osmotic stimulus showed a decrease in sympathetic activity not observed in normohydrated animals. Overall, the results allow to assert that the centrally released VP plays an important role in the development of the simpatoexcitation raised by increased osmolarity, through an action on the PVN neurons.