Dissertations / Theses on the topic 'Paraventricular nucleus'
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1
Davison, Ian. "Integration by the hypothalamic paraventricular nucleus of stressful stimuli." Thesis, University of Bristol, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260655.
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Verkuyl, Jan Maarten. "Stress, corticosterone and GABAergic inhibition in the rat paraventricular nucleus." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/70710.
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Cao, Xiao Yan. "Excitatory actions of orexins in rat paraventricular nucleus of thalamus." Thesis, University of Ottawa (Canada), 2006. http://hdl.handle.net/10393/27232.
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The midline thalamic paraventricular nucleus (PVT) receives a unique orexinergic innervation. To address possible function, this investigation used patch clamp recordings in rat brain slice preparations to evaluate intrinsic properties of PVT neurons and neuronal responses to bath-applied orexin peptides (A and/or B). PVT neurons displayed distinct state-dependent burst or tonic firing patterns, time dependent and time-independent inward rectification, T-type currents and low threshold spikes, action potential after-hyperpolarizations, spike frequency adaptation and spike broadening. A majority responded to both orexin peptides with slowly rising and prolonged membrane depolarizations, and inward currents that involved closure of potassium channels and/or opening of nonselective cationic channels. These data imply that endogenously released orexins likely act at both types of orexin receptors that can engage two conductances to modulate and increase neuronal excitability in PVT, a role that may be important for 'arousal' and neurotransmission within this midline thalamic nucleus.
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Ho, Sze-ngar Sara. "Synaptic modulation by 5-hydroxytryptamine in the rat hypothalamic paraventricular nucleus." Click to view the E-thesis via HKUTO, 2005. http://sunzi.lib.hku.hk/hkuto/record/B3194341X.
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Ho, Sze-ngar Sara, and 何思雅. "Synaptic modulation by 5-hydroxytryptamine in the rat hypothalamic paraventricular nucleus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B3194341X.
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Follwell, Matthew J. "Effects of orexin A on hypothalamic paraventricular nucleus neurons of the rat." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63303.pdf.
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Borduas, Jean-Francois. "Modulation of Voltage-Gated Calcium Channels by Group II Metabotropic Glutamate Receptors in the Paraventricular Nucleus of the Thalamus." Thèse, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/19988.
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Compounds that interact with Group II metabotropic glutamate receptors (mGluRs) have antipsychotic effects in animal models. These drugs have also shown efficacy in the treatment of schizophrenia in humans. The mechanism of action is believed to arise from a reduction of glutamatergic transmission in limbic and forebrain regions commonly associated with this disorder. Previous anatomical tracer and lesion studies have revealed that neurons of the paraventricular nucleus of the thalamus (PVT) are an important source of the glutamatergic drive to these specific regions. However, the function of Group II mGluRs in the PVT remains to be determined. Whole-cell recordings from PVT neurons reveal that activation of these receptors has two interesting effects; it reduces calcium entry through voltage-gated calcium channels and it causes neurons to hyperpolarize. These two effects may contribute to affect the excitability of PVT neurons, an action that may underlie the effectiveness of Group II mGluR-activating compounds.
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Clark, Andrew J. M. "On the action of noradrenaline microinjected into the paraventricular nucleus of rat hypothalamus." Thesis, University of St Andrews, 1990. http://hdl.handle.net/10023/14704.
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The microinjection of noradrenaline (NA) into the hypothalamic paraventricular nucleus (PVN) of the rat results in feeding. This response was shown; contrary to previous reports; to be mediated through both a-1 and a-2 NA receptors. Selective blockade of these two receptor sub-types, in conjunction with re-uptake blockade was used to examine the individual contributions of each receptor type to the whole response. It is suggested that the previously reported a-2 receptor specificity of the response to microinjected NA is a result of the location of these receptors. The post-synaptic a-1 receptor being located close to the pre-synaptic re-uptake mechanism, whilst the post-synaptic a-2 receptor is located outside the synapse and thus away from the re-uptake mechanism. The re-uptake mechanism acts to create a concentration difference of microinjected NA between the two receptor sub-types, resulting in a higher concentration and thus a preferential action at a-2 receptors. The involvement of the paraventricular NA system in stress induced eating was examined using a tail pinch procedure. Microinjection of NA antagonists into PVN prior to the onset of the pinch had no effect on the duration or latency of the eating response, thus there was no evidence for the involvement of this system in tail pinch elicited feeding. Further to the suggestion that the NA a-2 receptor is extra-synaptic whilst a-1 is intrasynaptic, the actions of NA were examined at a second site. NA microinjected into the ventral striatum elicited a vigorous locomotor response, although the origins of this showed a clear priming effect. However, this response was unaffected by prior microinjection of NA a-antagonists, preventing an analysis of receptor involvement comparable with that performed in PVN.
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Bains, Jaideep S. "Nitric oxide driven inhibitory neurotransmission in the paraventricular nucleus, evidence for ultra-short-loop feedback." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/nq22443.pdf.
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Mueller, Heather. "Depressor and diuretic effects of imidazoline receptor stimulation in the paraventricular nucleus of the hypothalamus." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0007/MQ41750.pdf.
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Dearden, Laura Ann. "Nutrient-mediated transcriptomes in the Paraventricular Nucleus of the Hypothalamus : dynamic regulation and downstream physiology." Thesis, University of Bristol, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.633156.
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The obesity epidemic has fuelled research into the etiology of this complex disorder, including lifestyle, genetic vulnerability and more recently the in utero environment. Exposure to maternal obesity in utero programs metabolic dysfunction in offspring, however the mechanisms are unknown. Little is known about how the CNS senses, integrates and translates nutrient information into adjustment of neuronal and ultimately physiological function. The PVH is critical for maintaining energy- and glucosehomeostasis, but the molecular mechanisms underpinning this action remain unknown. We hypothesised that a PVH nutrient-sensitive transcriptome is critical in mediating adjustment of metabolic state, and that disruption of the PVH nutrient-mediated transcriptome may underpin physiological phenotypes in offspring exposed to an adverse in utero environment.
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Anonuevo, Adam Manuel Smith. "Local and distal origins of limbic-related projections to the paraventricular nucleus of the hypothalamus." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/44997.
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Cortico-limbic circuits are often activated in response to emotional stress to provide salient information about individual stimuli. This allows organisms to recruit adequate response mechanisms, one of which is the hypothalamic-pituitary-adrenal axis. Cellular groups directly adjacent to the paraventricular nucleus of the hypothalamus (PVN) are in position to integrate and relay cortico-limbic projections to the PVN directly. Using a neuroanatomical approach we discovered unique patterns and strengths of cortico-limbic projections to separate cell groups in the PVN surround. Further, in response to restraint stress, dual retrograde labeling with the cellular activation marker FOS suggests these PVN surround circuits are involved in adaptive responses to emotional stress. Of the PVN surround subregions, the zona incerta (ZI) showed particularly dense connectivity with the medial prefrontal cortex (mPFC), lateral septum, and paraventricular thalamus. Due to the strength of this connectivity we sought to confirm that it can act as a relay site to the PVN through targeted injections of anterograde tracer. ZI injections of anterograde tracer led to terminally labeled fibers in the PVN confirming the capacity to influence hypophysiotropic neurons of the PVN. Additionally, there is the potential for the ZI to share functional cross-talk with other PVN surround subregions. In our final experiment we directed injections of retrograde tracer into the PVN in concert with anterograde injections in the mPFC resulting in convergence of tracer labeling within the ZI. The abutted signals strongly indicate the PVN surround is a promising site for limbic influence on HPA.
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Cham, Joo Lee, and julie cham@rmit edu au. "The role of the hypothalamic paraventricular nucleus in the cardiovascular responses to elevations in body temperature." RMIT University. Medical Sciences, 2008. http://adt.lib.rmit.edu.au/adt/public/adt-VIT20080805.114529.
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The hypothalamic paraventricular nucleus (PVN) is known to be a major integrative region within the forebrain. It is composed of functionally different subgroups of neurons, including the parvocellular neurons that project to important autonomic targets in the brainstem e.g. the rostral ventrolateral medulla (RVLM) and the intermediolateral cell column (IML) of the spinal cord, where the sympathetic preganglionic motor-neurons are located. These regions are critical in cardiovascular regulation; hence, these projections are likely to mediate the effects of the PVN on sympathetic nerve activity and hence may contribute to the cardiovascular changes induced by physiological stimuli such as elevations in body temperature. The neurotransmitter such as nitric oxide (NO) is important in cardiovascular regulation and it is now emerging as a major focus of investigation in thermoregulation. One of the most striking accumulations of NO containing-neurons is in the PVN where it appears to be playing an important role in cardiovascular regulation and body fluid homeostasis. The results of the work show; 1. That spinally-projecting and nitrergic neurons in the PVN may contribute to the central pathways activated by exposure to a hot environment. 2. Suggests that nitrergic neurons and spinally- projecting neurons in the brainstem may make a small contribution to the central pathways mediating the reflex responses initiated by hyperthermia. 3. The present study also illustrates that these PVN neurons projecting to the RVLM may make a smaller contribution than the spinal-projecting neurons in the PVN to the cardiovascular responses initiated by heat. 4. The results of my studies showed that the microinjection of muscimol to inhibit the neuronal activity in the PVN abolished the reflex decrease in renal blood flow following an elevation of core body temperature. In addition, this effect was specific to the PVN, since microinjections of muscimol into areas outside the PVN were not effective. These findings demonstrate that the PVN is critical for this reflex cardiovascular response initiated by hyperthermia. In conclusion, PVN is critical for the reflex decrease in renal blood flow during elevations in core body temperature. We hypothesise that projections from the PVN to the spinal cord and the RVLM contribute to the reflex cardiovascular responses. Additionally, nitrergic neurons in the PVN may contribute but the physiological role of those neurons in the reflex responses elicited by hyperthermia needs to be investigated.
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Jiang, Ying. "Fasting alters histone methylation in paraventricular nucleus of chick through regulating of polycomb repressive complex 2." Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/51751.
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The developing brain is highly sensitive to environmental influences. Unfavorable nutrition is one kind of stress that can cause acute metabolic disorders during the neonatal period [1,2,3] and severe diseases in later life [4,5]. These early life experiences occurring during heightened periods of brain plasticity help determine the lifelong structural and functional aspects of brain and behavior. In humans, for example, weight gain during the first week of life increased the propensity for developing obesity several decades later [5]. This susceptibility is, if not all, related to the dynamic reversible epigenetic imprints left on the histones [6,7,8], especially during the prenatal and postpartum period [9].
Histones are highly dynamic and responsive towards environmental stress [10,11]. Through covalent modification of the histone tail, histones are able to direct DNA scaffolding and regulate gene expression [10,12]. Thus far, various types of post translational modifications have been identified on various histones tails [12]. Among them, the methylation and acetylation on lysine residue (K) 27 on histone 3 (H3) has been tightly linked to gene repression [13,14] and activation [15], respectively. EZh2 (enhancer of zeste 2) in the polycomb repressive complex 2 (PRC2) is the only methyltransferase that has been linked to catalyze this methylation reaction. In addition, SUZ (suppressor of zeste) and EED (embryonic ectoderm development) are two other key proteins in PRC2 function core that help EZH2. As previous reported, increased H3K27 methylation was monitored after fasting stress during neonatal period in chicks' paraventricular nucleus (PVN). In this study, we investigated the detailed mechanism behind changes in H3K27 methylation following fasting stress.
After 24 hours fasting on 3 days-of-age (D3), chicks exhibited elevated mRNA levels of PRC2 key components, including EZH2, SUZ and EED, in the PVN on D4. Western blots confirmed this finding by showing increased global methylation status at the H3K27 site in the PVN on D4. In addition, until 38 days post fasting, SUZ and EZH2 remained inhibited. A newly identified anorexigenic factor, Brain-derived neurotrophic factor (BDNF), was used as an example of multiple hormones expressed in PVN to verify this finding. Both BDNF protein and mRNA exhibited compatible changes to global changes of tri- (me3) and di-methylated (me2) H327. Furthermore, by using chromatin immunoprecipitation assays (ChIP), we were able to monitor the changes of H3K27me2/me3 deposition along the Bdnf gene. Fasting significantly increased H3K27me2/me3 as well as EZH2 at the Bdnf's promoter, transcription start site and 3'-untranslated region. These data show that fasting stress during the early life period could leave epigenetic imprinting in PVN for a long time. Next, we tried to understand the function of this epigenetic imprinting in the chicks' PVN. Thus, we compared naive chicks (never fasted) to chicks that received either a single 24 hour fast on D3 or two 24 hour fast on both D3 and 10 days-of-age (D10). We found that the D3 fasted group significantly increased the level of PRC2 key components and its product H3K27me2/me3 compared to the naive group. However, D3 fasting and D10 fasting together decreased the surges of H3K27me2/me3, SUZ and EED (not EZH2) compared to the naive group. We called this phenomenon "epigenetic memory". The Western blot, qPCR and CHIP assay results from BDNF all confirmed the existence of "epigenetic memory" for PRC2. These data suggested that fasting stress during the early period of brain development could leave long term epigenetic modifications in neurons. These changes could be beneficial to the body, which keeps homeostasis of inner environment and prevent massive response to future same stress.
The EZH2 protein was knocked down and the H3K27 methylation status changes were monitored after applying the same treatment. We first confirmed that EZH2 antisense oligonucleotides (5.5 ug), but not EZH2 siRNA and artificial cerebrospinal fluid (ACSF), inhibit EZH2 protein by 86 % in the PVN. Then, on D3, chicks were subjected to a 24 hour fasting stress (D3-fasting) post either EZH2 antisense or ACSF injection. The EZH2 antisense blocked the surge of both EZH2 mRNA and H3K27 methylation after D3-fasting. At the same time, BDNF exhibited elevated expression levels and less methylated H3K27 deposition along the Bdnf gene. In addition, we were also interested in the changes of "epigenetic memory" post EZH2 antisense injection. We found that after EZH2 antisense injection, chicks' PVN no longer exhibited any "epigenetic memory" to repetitive fasting stress. While EZH2 mRNA was constantly inhibited, SUZ, EED and H3K27me2/3 levels were unpredictable. These findings suggested that neurons in the PVN utilized PRC2 as a major H3K27 methylation tool. Knockdown of EZH2 in the PRC2 impaired the proper response in PVN to fasting stress and PVN's ability to acclimate to repetitive fasting stresses. Thus, EZH2 is an important H3K27 methyltransferase inside chicken hypothalamus to maintain homeostasis.
In conclusion, fasting stress during the early life period could leave epigenetic markers on chromosomes of neurons in the feeding regulation center. These epigenetic markers will be left on chromosomes for a long period of time and have a beneficial role in keeping homeostasis when individuals face future fasting stress again. H3K27 methylation is one of these epigenetic markers and inhibits expression of various genes inside neurons. EZH2 is so far the only detected methyltransferases for H3K27 that form the PRC2. Thus EZH2 plays a key function in the body's response to fasting.Ph. D.
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Semple, Erin A. "Hypothalamic Melanocortin 4 Receptors Regulate Sexual Behavior in Mice." University of Toledo Health Science Campus / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=mco1500720484755042.
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Cork, Simon Christopher. "Altered NMDA and GABA-A receptor subunit expression in the hypothalamic paraventricular nucleus of hypertensive and pregnant rats." Thesis, Durham University, 2013. http://etheses.dur.ac.uk/7275/.
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Hypertension and pregnancy are both accompanied by increases in sympathetic nerve activity. This has been attributed in part, to changes in the neurochemistry of the hypothalamic paraventricular nucleus (PVN). In hypertension, physiological studies have revealed that decreases in GABAergic inhibition and increases in glutamatergic excitation within the PVN contribute to this sympathoexcitation. In late-term pregnancy however, the sympathoexcitation appears to be mediated by decreases in GABAergic inhibition, with no glutamatergic contribution. This study aimed to examine the molecular characteristics of the GABAA and NMDA receptor to ascertain whether changes in their subunit expression in the PVN could contribute to the sympathoexcitation observed in these physiological states. Whole PVN micropunches subjected to quantitative immunoblotting were combined with semi-quantitative analysis of immunohistochemistry to ascertain which subunits were altered, and whether the alteration was confined to specific parvocellular subnuclei of the PVN. The results of this study show that both hypertension and pregnancy are accompanied by significant decreases in both the α1 and α5 subunit of the GABAA receptor in the PVN. Furthermore, hypertension is also accompanied by a significant increase in the expression of the GluN2A subunit of the NMDA receptor, which was associated with increases in the number of GluN2A-immunoreactive neurones in specific parvocellular subnuclei of the PVN. Conversely, pregnancy was associated with a significant increase in GluN2B subunit expression which was not associated with changes in cell immunoreactivity in any parvocellular subnuclei. The results from this study suggest that decreases in α1 and α5 subunits of the GABAA receptor may be important in mediating the sympathoexcitation observed in both of these physiological states, with the greater level of sympathoexcitation observed in hypertension possibly attributed to increases in GluN2A-mediated NMDA receptor expression.
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Feetham, Claire. "The role of the paraventricular nucleus of the hypothalamus in the central control of the autonomic nervous system." Thesis, University of Liverpool, 2014. http://livrepository.liverpool.ac.uk/2007920/.
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The paraventricular nucleus (PVN) is a region of the hypothalamus considered the “master controller” of the autonomic nervous system. A subregion of the PVN, the parvocellular subnucleus, is believed to be involved in autonomic control, but its physiological importance is not fully understood. This thesis aimed to investigate the role of the parvocellular PVN in autonomic control and the underlying mechanisms responsible. In slice cell-attached patch action current recordings showed that putative parvocellular neurones are sensitive to osmolality and that a member of the mechanosensitive transient receptor potential ion channel (TRP) family TRPV4 plays a role in this osmosensing. TRPV4 agonists gave a similar reduction in action current frequency (ACf) to hypotonic challenge, which was reversed by selective TRPV4 inhibitors. Single-channel recordings identified a TRP-like channel on parvocellular neurones, and the activity of this channel was increased by the TRPV4 agonist 4αPDD. Intracellular calcium recordings showed increases in Ca2+ in response to either hypotonic challenge or 4αPDD. Furthermore, a role for TRPV4 was verified in central osmosensing at the whole animal level; central injections of hypotonic solution decreased blood pressure; an effect ablated by a TRPV4 inhibitor. Functional coupling between TRPV4 channels and Ca2+-activated K+ (KCa) channels was also explored. The effect of hypotonic challenge was reversed by inhibition of the small-conductance KCa (SK) channel. Since the effects of TRPV4 could also be blocked by an SK inhibitor, it is proposed that TRPV4 is coupled to SK to modulate neuronal activity. During calcium recordings Aaplication of a TRPV4 agonist in the presence of an SK inhibitor showed a reduced, but sustained Ca2+ rise compared to TRPV4 agonist application alone, suggesting feedback mechanisms are also in play. These mechanisms were also verified, quantitatively, with a mathematical model written in the NEURON simulation environment and incorporating experimentally derived parameters. A role for this area of the PVN in temperature sensing was also discovered, with ACf decreasing with an increase in temperature from 25oC to 37oC. Pharmacological investigation identified another TRP channel, TRPM2, to be central for the PVN response to temperature. ECG recordings from rats implanted with telemeters confirmed roles for neurokinin 1 receptor (NK1) expressing neurones in the PVN in the cardiovascular response to psychological stress and in the setting of circadian heart rate. Heart rate variability analysis showed that increases in the sympathetic activity indicator, “LF/HF”, in response to handling stress were ablated by specific lesioning of the NK1 neurones in the PVN. In addition these animals had a significant shift in the daily variation of their average day/night heart rate. In conclusion this thesis identifies the mechanisms underlying several different functional roles for parvocellular PVN neurones and indicates the PVN may be a multifunctional homeostatic “detector”.
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黃德彬 and Tak-pan Wong. "An electrophysiological study of the projection from the paraventricular nucleus of hypothalamus to the cardiovascular neuronsin the rostral ventrolateral medulla of the rat." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1994. http://hub.hku.hk/bib/B31212724.
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Wong, Tak-pan. "An electrophysiological study of the projection from the paraventricular nucleus of hypothalamus to the cardiovascular neurons in the rostral ventrolateral medulla of the rat /." Hong Kong : University of Hong Kong, 1994. http://sunzi.lib.hku.hk/hkuto/record.jsp?B14709120.
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Sonner, Patrick M. "FUNCTIONAL INTERPLAY BETWEEN SUBTHRESHOLD ION CHANNELS IN PREAUTONOMIC NEURONS OF THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS IN HEALTH AND DISEASE CONDITIONS." Wright State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=wright1197577443.
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Santos, Patricia Rabelo dos. "Expressão do fator de transcrição nuclear kB (NF-kB) em neurônios ocitocinérgicos de ratos submetidos à sobrecarga salina : influência da dexametasona." Universidade Federal de Sergipe, 2014. https://ri.ufs.br/handle/riufs/4004.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPESThe hypothalamic-neurohypophysial system is the main system through which the brain maintains homeostasis of bodily fluids. Specifically, the supraoptic (SON) and paraventricular (PVN) hypothalamic nuclei are directly involved with hydroelectrolytic equilibrium and are specialized in the synthesis and secretion of vasopressin and oxytocin (OT). Changes in the milieu intérieur are conceived as stressors by the central nervous system (CNS) and are modulated by the hypothalamic-pituitary-adrenal axis (HPA). Nuclear transcription factor kappa B (NF-κB) mediates immunosuppressant and anti-inflammatory of glucocorticoids. Thus, the aim of this study was to verify the expression profile of component p65 of the NF-κB classical pathway in SON and PVN oxytocinergic neurons in response to dehydration, glucocorticoid treatment, and in normal conditions. Methods: Wistar rats (250-300g) were maintained in controlled environment with temperature (23 ± 2ºC), light/dark cycle of 12 hours and water and food specific for rodents ad labitum until the beginning of experimental period. All procedures were approved by Ethical Comitee of Research with Animals from UFS (Protocol # 60/2012). Animals were grouped into Control (water ad libitum for 4 days, n = 6-7); Control + Dexa (water ad libitum and treated with dexamethasone, n = 6-7); SL4 (salt overloading ad libitum, 1.8% NaCl for 4 days, n = 6-7); SL4 + Dexa (salt overloading ad libitum, 1.8% NaCl for 4 days and dexamethasone, n = 6-7). Dexamethasone (10 mg/kg i.p.) was administered 12 and 2 hours before perfusion and removal of brains for OT/p65 immunofluorescence, or before sacrifice for blood sampling and angiotensin II (ANGII) dosage. We applied two-way ANOVA and Bonferroni posthoc test to analyze behavioral and hormonal dosage data. Results obtained from imunohistochemestry for evaluation of oxytocin and/or p65 neuronal activity, were subjected to qualitative evaluation. We verified SL4 animals ingested more fluid than control, on second (p<0.01), third (p<0.01) and forth (p<0.001) experimental day. SL4 also increased plasmatic concentration of ANGII (p<0.01). Qualitative analysis of double labeling OT/p65 on PVN and SON revealed a weak immunoreactivity for oxytocin on SL4 and SL4 + Dexa groups, when compared to control and Control + Dexa groups. Was observed expression of p65 subunit of NF-κB in all hypothalamic studied areas, with predominant cytoplasmic imunoreactivity in all groups. These data demonstrate that p65 subunit of NF-κB are present in oxytocinergic neurons from the most important hypothalamic areas that integrates the stress axis (HPA) and hidroelectrolyte balance (SHNH). More studies are necessary to clarify the real participation of NF-κB intracellular pathway evoked by intracellular dehydration on endocrines and behavioral hidroelectrolyte adjustments.
O sistema hipotálamo neuro-hipofisário (SHNH) é o principal sistema pelo qual o cérebro mantém a homeostase dos líquidos corporais. Especificamente, os núcleos supra-óptico (SON) e paraventricular (PVN) do hipotálamo estão diretamente envolvidos com o controle do balanço hidroeletrolítico e são especializados na síntese e secreção de vasopressina (AVP) e ocitocina (OT). Alterações no milieu intérieur são vistas como estressoras pelo sistema nervoso central (SNC) e moduladas pelo eixo hipotálamo-hipófise-adrenal (HHA). O fator de transcrição nuclear kappa B (NF-κB) é conhecido por mediar os efeitos imunossupressores e anti-inflamatórios dos glicocorticoides. Sendo assim, o objetivo do presente estudo foi verificar o perfil de expressão do componente p65 da via clássica do NF-κB em neurônios ocitocinérgicos do PVN e SON, em resposta à desidratação crônica, associada, ou não, ao tratamento com glicocorticoides. Métodos: Ratos wistar (250-300 g) foram mantidos em ambiente com temperatura (23 ± 2ºC) e luminosidade, ciclo claro-escuro de 12 horas (luz das 6 às 18 horas), controladas, com água e ração específica para roedores (Labina®- Purina) ad libitum até o início dos experimentos. Todos os procedimentos foram aprovados pelo Comitê de Ética em Pesquisa com Animais da UFS (Protocolo # 60/2012). Os animais foram divididos de modo a constituir os grupos Controle (ratos com acesso à água ad libitum, durante quatro dias, n = 6 - 7); Controle + Dexa (ratos com acesso à água ad libitum, durante quatro dias, e tratados com dexametasona, n = 6 - 7); SL4 (ratos com acesso à sobrecarga salina ad libitum, solução de NaCl 1,8%, durante quatro dias, n = 6 - 7); SL4 + Dexa (ratos com acesso à sobrecarga salina ad libitum, NaCl 1,8%, durante quatro dias e tratados com dexametasona, n = 6 - 7). A dexametasona (10 mg / kg, i.p.) foi administrada apenas no 4º dia, 12h e 2 h antes da perfusão para coleta do cérebro e realização da dupla imunofluorescência OT/p65 ou eutanásia para coleta de sangue do tronco e posterior dosagem de angiotensina II (ANGII). Os dados comportamentais e de dosagem hormonal obtidos foram submetidos ao teste ANOVA de duas vias e pós-teste Bonferroni. Os resultados obtidos da imuno-histoquímica, para a marcação de neurônios expressando ocitocina e/ou p65, foram submetidos à avaliação qualitativa. Verificou-se que os animais SL4 ingeriram mais fluido que seus controles, no segundo (p < 0,01), terceiro (p < 0,001) e quarto (p < 0,001) dia experimental. A SL4 elevou a concentração plasmática de ANGII (p < 0,01). A análise qualitativa da dupla imunofluorescência OT/p65 no PVN e SON revelou uma fraca imunorreatividade à ocitocina nos grupos SL4 e SL4 + Dexa, quando comparados aos grupos Controle e Controle + Dexa. Observou-se expressão da subunidade p65 do NF-κB em todas áreas hipotalâmicas estudadas, com imunorreatividade predominantemente citoplasmática em todos os grupos. Estes dados mostram que a subunidade p65 do NF-κB está presente em neurônios ocitocinérgicos das principais áreas hipotalâmicas que integram os eixos do estresse (HHA) e do equilíbrio hidroeletrolítico (SHNH). Mais estudos são necessários a fim de esclarecer sobre a real participação da via intracelular do NF-κB evocada pela desidratação intracelular, nos ajustes hidroeletrolíticos endócrinos e comportamentais.
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Silva, Ana Luísa Aires da. "Influence of sex and gonadectomy in the anatomy and neurochemical organization in the dorsal parvicellular division of the hypothalamic paraventricular nucleus." Dissertação, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/50171.
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Silva, Ana Luísa Aires da. "Influence of sex and gonadectomy in the anatomy and neurochemical organization in the dorsal parvicellular division of the hypothalamic paraventricular nucleus." Master's thesis, Faculdade de Medicina da Universidade do Porto, 2009. http://hdl.handle.net/10216/50171.
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Wolfe, Farah. "Role of the hypothalamus in sociality : possible contribution to autism spectrum disorders." Thesis, Aix-Marseille, 2016. http://www.theses.fr/2016AIXM5058.
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La sociabilité de l’homme est un phénomène complexe. Les théories dominantes essayant d'expliquer les mécanismes neurobiologiques de cette sociabilité ont largement impliqué l'ocytocine (OXT), un neuropeptide qui facilite de nombreuses fonctions et comportements sociaux. L'hypothalamus, parmi ses nombreuses fonctions, synthétise et sécrète l’OXT via son noyau supraoptique (SON) et le noyau paraventriculaire (PVN), faisant de lui un candidat intéressant pour comprendre les bases neurales de cette sociabilité. Dans cette thèse, qui combine trois études en imagerie par résonance magnétique (IRM), nous avons examiné 1) les différences anatomiques au sein de l'hypothalamus entre des participants contrôles et des patients autistes; 2) l’activité de l'hypothalamus, et plus spécifiquement des sous-régions hypothalamiques incluant le SON et le PVN, en réponse à des visages portant différents niveaux de sociabilité; 3) les connections fonctionnelles que ces sous-régions hypothalamiques entretiennent avec d'autres réseaux cérébraux. Nos résultats révèlent une spécificité, tant dans leur activité fonctionnelle que dans leurs connections anatomiques, des deux sous-régions hypothalamiques (SON et PVN) en fonction du niveaux de sociabilité. Ce travail de thèse fournit donc non seulement de nouvelles méthodes pour explorer les petites sous-régions hypothalamiques mais confirme également le rôle de l’hypothalamus dans la sociabilité et ses anomalies, apportant ainsi un nouvel éclairage sur l’origine des dysfonctionnements sociaux dans l’autisme et d'autres pathologiesHuman sociality is a complex phenomenon. Prevailing theories attempting to explain the neurobiological mechanisms of human sociality have implicated neuropeptide oxytocin (OXT), which facilitates numerous social functions and behaviors. The hypothalamus, among its many functions, also synthesizes and secretes OXT via its supraoptic nucleus (SON) and the paraventricular nucleus (PVN), making them viable candidates to understand the underpinnings of various social processes. This thesis combines three magnetic resonance imaging (MRI) studies investigating 1) anatomical difference of the hypothalamus between neurotypics and patients with Autism Spectrum Disorders (ASD); 2) functional MRI of the hypothalamus, specifically in hypothalamic subregions containing SON and PVN in response to faces of individuals with varying social significance; 3) functional connectivity of these hypothalamic subregions to other brain networks. Results revealed differential activity of hypothalamic subregions in response to various faces and distinctive patterns of connectivity to other brain areas that are involved in social cognition, as well as anatomical abnormalities of the hypothalamus in ASD. Altogether, the work in this thesis provides novel methods of measuring small hypothalamic subregions and supporting evidence of hypothalamic involvement in social functions that may also shed some light on social dysfunctions in ASD and other pathologies
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Jolousjamshidi, Banafsheh. "Investigating the Effects of Polychlorinated Biphenyls on Circulating Oxytocin Levels, Area of the Paraventricular Nucleus and Social Behavior in Juvenile Male Rats." Bowling Green State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1182719734.
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Carmichael, II Samuel Paterson. "HYPOTHALAMIC MEDIATION OF ACUTE INCREASES IN ARTERIAL BLOOD PRESSURE AND RENAL SYMPATHETIC NERVE ACTIVITY DURING ELECTRICAL STIMULATION OF THE LAMINA TEMRINALIS." UKnowledge, 2008. http://uknowledge.uky.edu/gradschool_theses/513.
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Discrete electrical stimulation of the organum vasculosum of the lamina terminalis (OVLT) produces sympathetically-mediated increases in peripheral resistance and arterial blood pressure (ABP). Since efferent fibers from the lamina terminalis innervate the kidney through polysynaptic connections, the present study determined whether electrical stimulation of the OVLT increased sympathetic outflow to the kidney. In anesthetized male, Sprague-Dawley rats (n=5) electrical stimulation of OVLT neurons produced frequency and current intensity dependent increases in renal sympathetic nerve activity (RSNA) and ABP that were abolished by ganglionic blockade with the nicotinic antagonist chlorisondamine (5mg/kg,i.v.). Since neurons from the OVLT terminate within the hypothalamic paraventricular nucleus (PVH), the present study also determined whether these connections mediate a portion of sympathetic and pressor responses to electrical stimulation of the OVLT. Bilateral inhibition of the PVH with the GABAA agonist muscimol (5mM/100nl) significantly attenuated the increase in ABP at all frequencies and current intensities. Spike-triggered averaging of RSNA revealed that PVH inhibition significantly blunted the RSNA responses to OVLT stimulation at 100, 200, but not 400andamp;igrave;A. The present findings indicate that electrical stimulation of the OVLT increases RSNA and ABP and that these responses are partially mediated by the tonic activity of PVH neurons.
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Silva, Talita de Melo e. "Integração entre o bulbo ventrolateral rostral e o núcleo paraventricular do hipotálamo durante a ativação dos quimiorreceptores arteriais: possível envolvimento dos mecanismos catecolaminérgicos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-11082016-135021/.
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A redução na pressão parcial de O2 é detectada pelos quimiorreceptores periféricos que sinalizam ao sistema nervoso central para que haja uma correção na homeostasia. Estudos neuroanatômicos mostram que neurônios C1 enviam projeções para núcleo paraventricular do hipotálamo (PVH), mas, pouco descrevem a participação desta via em uma situação de hipóxia. Ademais, o envolvimento de mecanismos neuroimunes no controle neural cardiorrespiratório durante a hipóxia não está esclarecido. Neste estudo mostramos que neurônios catecolaminérgicos do BVLr/C1 ativados por hipóxia se projetam para o PVH, e que a integridade destes neurônios é essencial para que neurônios do PVH sejam ativados por hipóxia. Além disso, o tratamento com minociclina alterou a expressão de mediadores inflamatórios no BVLr e PVH, a expressão de Fos e as repostas respiratória e autônoma desencadeadas pela hipóxia. Estes resultados conferem uma importante caracterização sobre a distribuição dos neurônios catecolaminérgicos do BVLr/C1 que são ativados por hipóxia e se projetam para o PVH. Além de mostrar que a hipóxia pode desencadear mecanismos neuroimunes que possivelmente envolvem a participação da microglia e também recrutam a via neural C1- PVH.The reduction in the O2 partial pressure is detected by the peripheral chemoreceptors that send information to central nervous system to correct the homeostasis. Neuroanatomical studies show that C1 neurons send projections to the paraventricular hypothalamic nucleus (PVH), but rather describe the involvement of this pathway in a hypoxic situation. Furthermore, the potential involvement of neuroimmune mechanisms in cardiorespiratory neural control during hypoxia is unclear. In this study we show that catecholaminergic neurons localized in rostral ventrolateral medulla (RVLM) / C1 cells activated by hypoxia send projections to the PVH, and the integrity of these neurons is essential for PVH neurons be activated by hypoxia. Moreover, treatment with Minocycline changed the expression of inflammatory mediators in RVLM and PVH, the expression of Fos in these nucleus, and respiratory and autonomic responses elicited by hypoxia. These findings provide an important characterization of the distribution of catecholaminergic RVLM / C1 neurons that are activated by hypoxia and project to the PVH. In addition to showing that hypoxia can trigger neuroimmune mechanisms that possibly involve the microglia activity and also recruit the C1/PVH neural pathway.
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Núñez, Parra María Cristina. "Caracterización de los cambios celulares y moleculares en el sistema cerebral del estrés durante la dependencia de morfina / Cellular and molecular changes in the stress-responsive system during morphine dependence." Doctoral thesis, Universidad de Murcia, 2008. http://hdl.handle.net/10803/10800.
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Morphine withdrawal increases the HPA axis activity, which is dependent on a hyperactivity of noradrenergic pathways (NTS-A2) innervating the PVN. In this Thesis we found that morphine withdrawal resulted in an increase in ACTH and corticosterone secretion and a neuronal activation in the PVN. Additionally, we found robust increases in CRF and AVP hnRNAs in the PVN, concomitantly with an increase in c-Fos expression. Morphine withdrawal activated ERK1/2 in PVN and NTS, which could be involved in the c-Fos expression. Morphine withdrawal induced an increase in TH mRNA levels in the NTS-A2, total TH protein in the NTS and TH phosphorylation at Ser31 in PVN and NTS-A2, which resulted in an augmentation of TH activity in the PVN. The enhancement in TH phosphorylated at Ser31 was blocked by SL327 in both nuclei. Finally, we have found that adrenalectomy eliminated the hyperactivity of noradrenergic pathways innervating the PVN during morphine withdrawal.La abstinencia a morfina aumenta la actividad del eje HHA, que depende de la hiperactivación de las vías noradrenérgicas (NTS-A2) que inervan al PVN. En esta Tesis encontramos que la abstinencia a morfina induce la liberación de ACTH y corticosterona y la activación neuronal del PVN. Además, observamos un aumento en los niveles de hnRNA para CRF y AVP en el PVN, concomitantemente con un incremento en la expresión de c-Fos. El síndrome de abstinencia a morfina activó a ERK1/2 en PVN y NTS. También indujo un incremento en el mRNA para TH en el NTS-A2, proteína TH total y fosforilación de TH en su Ser31 en PVN y NTS-A2, que se tradujo en un aumento en su actividad enzimática. El aumento de TH fosforilada en Ser31 fue bloqueado por SL327. Finalmente, la adrenalectomía eliminó la hiperactividad de las vías noradrenérgicas que inervan al PVN durante la abstinencia a morfina.
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Gabor, Alexander. "Role of Angiotensin II, Glutamate, Nitric Oxide and an Aldosterone-ouabain Pathway in the PVN in Salt-induced Pressor Responses in Rats." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/22900.
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High salt intake contributes to the development of hypertension in salt-sensitive humans and animals and the mechanistic causes are poorly understood. In Dahl salt-sensitive (S) but not salt-resistant (R) rats, high salt diet increases cerebrospinal fluid (CSF) [Na+] and activates an aldosterone-mineralocorticoid receptor-epithelial sodium channel-endogenous ouabain (MR-ENaC-EO) neuromodulatory pathway in the brain that enhances the activity of sympatho-excitatory angiotensinergic and glutamatergic pathways, leading to an increase in sympathetic nerve activity (SNA) and blood pressure (BP). We hypothesize that high salt diet in Dahl S rats enhances Ang II release in the paraventricular nucleus (PVN), causing a decrease in local nitric oxide (NO) action and an increase in local glutamate release thereby elevating SNA, BP and heart rate (HR). The present study evaluated the effects of agonists or blockers of MR, ENaC, EO, nitric oxide synthase (NOS) or glutamate and AT1-receptors on the BP and HR responses to acute infusions of Na+ rich aCSF, intracerebroventricularly (icv), or in the PVN of Dahl S, R or Wistar rats or to high salt diet in Dahl S and R rats. In Wistar rats, aldosterone in the PVN enhanced the BP and HR responses to infusion of Na+ rich aCSF in the PVN, but not in the CSF, and only the enhancement was prevented by blockers of MR, ENaC and EO in the PVN. AT1-receptor blockers in the PVN fully blocked the enhancement by aldosterone and the responses to infusion of Na+ rich aCSF icv, or in the PVN. Na+ rich aCSF in the PVN caused larger increases in BP and HR in Dahl S vs. R rats and the responses to Na+ were fully blocked by an AT1-receptor blocker in the PVN. BP and HR responses to a NOS blocker in the PVN were the same, but L-NAME enhanced Na+ effects more in Dahl R than S rats. High salt diet attenuated increases in BP from L-NAME in the PVN of Dahl S but not R rats. AT1 and glutamate receptor blockers candesartan and kynurenate in the PVN decreased BP in Dahl S but not R rats on high salt diet. At the peak BP response to candesartan, kynurenate in the PVN further decreased BP whereas candesartan did not further decrease BP at the peak BP response to kynurenate. Our findings indicate that both an acute increase in CSF [Na+] and high salt intake in Dahl S rats increases AT1-receptor activation and decreases NO action in the PVN thereby contributing to the pressor responses to Na+ and presumably, to dietary salt-induced hypertension. The increased BP response to AT1-receptor activation in the PVN of Dahl S is mediated by enhanced local glutamate receptor activation. An MR-ENaC-EO pathway in the PVN can be functionally active and further studies need to assess its role in Dahl S rats on high salt intake.
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Ramirez, Nuñez Wilson Ranú 1973. "Mecanismos neurais envolvidos no retardo do esvaziamento gástrico de íiquidos em ratos induzido através do infarto recente do miocardio." [s.n.], 2004. http://repositorio.unicamp.br/jspui/handle/REPOSIP/309176.
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Orientador: Eros Antonio de AlmeidaTese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: O esvaziamento gástrico (EG) consiste na transferência ordenada do conteúdo do estômago para o duodeno, Situações patológicas como alterações hemodinâmicas modificam a velocidade do E.G. e função motora do trato gastrointestinal. O infarto do miocárdio determina retarde do E.G. em ratos, possivelmente pelo estresse causado pela ligadura da artéria coronária. O sistema nervoso central (SNC) afeta as funções motora e secretora gastrintestinais, frente a uma situação de estresse existe aumento da retenção gástrica (RG) induzindo o retarde do E.G. O sistema parassimpático pode estar envolvido neste fenômeno. Por outro lado o sistema simpático controla o E.G., interrompendo a motilidade e a secreção, frente a uma situação de estresse como a do infarto do miocárdio o retarde do E.G., pode estar relacionado à atuação desse sistema. O objetivo deste trabalho foi Avaliar complacência gástrica (CG) em ratos submetidos a infarto recente do miocárdio, participação do nervo vago, sistema nervos simpático, efeito da injeção intra-cerebro-ventricular de GABAb e efeito da lesão do núcleo paraventricular no retarde do EG observado no infarto recente do miocárdio em ratos. Utilizados ratos Wistar, machos, entre 220 - 300g, adaptados ás condições do laboratório, divididos em 3 grupos: grupo INF; grupo SH e grupo NA. Infarto realizado por ligadura da artéria coronária descendente anterior esquerda. Animais após cirurgia permaneceram em jejum alimentar recebendo água ad libitum. Vinte e quatro horas após foi avaliado EG de 1,5 ml/100g de peso do animal de uma refeição de prova (RP) salina marcada com fenol vermelho. EG foi avaliado indiretamente, através da determinação da % de retenção gástrica (RG) da RP, 10 min. após administração orogástrica. Resultados mostraram que para o estudo da complacência gástrica não houve diferença significativa de pressão intragástrica entre os três grupos, nos três pontos de medida da pressão intragástrica (PIG) e em complementação as CGs não apresentaram diferenças significativas quando comparados entre si. No estudo da Vagotomia subdiafragmatica houve diferença significativa das RG (%) entre os subgrupos SH+Sh vs SH+Inf, o subgrupo Vgx+Inf apresentou diferença significativa em relação ao subgrupo SH+Inf e não diferiu do subgrupo Vgx+Sh. Para o estudo do efeito da injeção intra-cerebro-ventricular de GABAb houve diferença significativa entre os grupos SH+Sal e SH+Bac e Inf+Sal e Inf+Bac. No estudo da Simpatectomia química, grupo Inf+Sal apresentou diferença significativa quando comparados aos ratos SH+Sal, e grupo Inf+Pra com grupo SH+Sal não apresentaram diferenças significativas. O grupo Inf+Pra e Inf+Sal apresentaram diferença significativa e ratos SH+Pra e SH+Sal apresentaram diferença significativa quando comparados, No estudo da lesão do Núcleo paraventricular houve diferença significativa das RG (%) entre os subgrupos SH+Sh vs SH+Inf, os grupos PVN+Inf e SH+Inf apresentaram diferença significativa. Conclusões: 1) infarto recente do miocárdio não induz modificações no tônus gástrico em ratos, 2) Existe participação do nervo vago no retarde do EG causado pelo infarto recente do miocárdio, 3) Retardo EG mostrado pelos ratos infartados tem participação, pelo menos em parte, dos receptores alpha-1 adrenérgicos do sistema nervos simpático. 4) Existe participação do núcleo paraventricular no retardo do EG induzido pelo infarto recente do miocárdio
Abstract: Gastric emptying (GE) is the orderly transfer of stomach contents into the duodenum, pathological situations as hemodynamic changes modify GE speed and motor function of the gastrointestinal tract. Myocardial infarction determines GE delayed in rats, possibly due to stress caused by coronary artery ligation. Central nervous system (CNS) affects gastrointestinal secretory and motor functions, in a stressful situation there is increased gastric retention (GR) inducing GE delay. Parasympathetic system may be involved in this phenomenon. On the other hand sympathetic nervous system controls GE, disrupting motility and secretion, compared to a stressful situation such as myocardial infarction, GE delay, may be related to performance of this system. The objective of this study was to evaluate gastric compliance (GC) in rats submitted to recent myocardial infarction, involvement of vagus nerve, sympathetic nervous system, intra-cerebro-ventricular of GABAb injectin effect and paraventricular nucleus lesion effect on GE delay observed in recent myocardial infarction in rats. Used male Wistar rats, between 220-300g, adapted to laboratory conditions, divided into three groups: INF, SH and NA groups. Infarction performed by left anterior descending coronary artery ligation. After surgery, animals were fasted receiving water ad libitum. Twenty four hours after was evaluated GE of 1.5ml/100g body weight of a saline test meal (TM) labeled with red phenol. GE was indirectly estimated by determining % of gastric retention (GR) of test meal. 10 min. after orogastric administration. Results showed that gastric compliance study there was no significant difference in intragastric pressure between the three groups, in the three points of measurement of intragastric pressure (IGP) and complementation in GC showed no significant differences when compared with each other. In subdiaphragmatic vagotomy study, significant difference of GR (%) between subgroups SH+Sh vs SH+Inf, subgroup Vgx+Inf significant difference in the subgroup SH+Inf and did not differ in subgroup Vgx+Sh. To study the effect of intracerebroventricular injection of GABAb significant difference between groups SH+Sal vs SH+Bac and Inf+Sal vs Inf+Bac. To study the chemical simpatectomy by prazosin, the Inf+Sal group showed significant difference when compared to SH+Sal rats, and the group Inf+Pra with SH+Sal group showed no significant difference. The group Inf+Pra and Inf+Sal showed significant differences and the rats SH+Pra and SH+Sal showed significant difference when compared, for the study of the lesion of paraventricular nucleus of GR significant difference (%) between subgroups SH+Sh vs SH+Inf, the group PVN+Inf and SH+Inf showed significant difference. Conclusions: 1) recent myocardial infarction does not induce changes in gastric tone in rats, 2) there is involvement of the vagus nerve in GE delay caused by recent myocardial infarction, 3) GE delayed in infracted rats have participation, at least in part, of alpha-1 adrenergic receptors of the sympathetic nervous system, 4) there is participation of the paraventricular nucleus of GE delayed induced by recent myocardial infarction
Doutorado
Ciencias Basicas
Doutor em Clínica Médica
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Santos, Isabelle Rodrigues dos. "Efeitos da terapia hormonal na resposta ao estresse em modelo animal de perimenopausa." Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/17/17134/tde-18072018-170631/.
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A perimenopausa é caracterizada como o período de transição da vida reprodutiva para a não reprodutiva em mulheres, e inicia-se com o aparecimento dos sintomas clínicos, prolongandose até um ano após a última menstruação. Esta fase é caracterizada pela ocorrência de ciclos menstruais irregulares, alterações na produção hormonal, bem como por mudanças comportamentais, neuroendócrinas e metabólicas, sendo o período de maior vulnerabilidade a desordens afetivas quando comparado às outras fases da vida. Apesar dos diversos estudos desenvolvidos acerca das manifestações destes sintomas durante a perimenopausa, ainda pouco se sabe a respeito das modificações na atividade do eixo hipotálamo-hipófise-adrenal (HPA) e da resposta ao estresse. O reagente químico diepóxido de 4-vinilciclohexeno (VCD) acelera o processo natural de atresia folicular, possibilitando estudos desta fase da vida reprodutiva. Assim sendo, sua aplicação em roedores constitui um excelente modelo experimental capaz de simular em animais o que ocorre durante a perimenopausa. Assim, os objetivos deste trabalho foram avaliar, neste modelo animal de perimenopausa: 1) as respostas endócrinas (corticosterona e progesterona) e neuroniais (atividade das subdivisões parvocelulares medial e posterior - PaMP e PaPo do núcleo paraventricular do hipotálamo (PVN) e do locus coeruleus - LC) ao estresse de contenção e 2) a influência da terapia hormonal sobre estas respostas. Para tanto, ratas Wistar receberam injeções subcutâneas de Óleo ou VCD por 15 dias consecutivos, a partir do 28° dia de vida. Ao redor do 56º ao 66º dia do início da administração de Óleo ou VCD, as ratas dos grupos a serem estressados receberam implantes subcutâneos de um pellet contendo placebo (PL), estradiol (E2), progesterona (P4) ou estradiol+progesterona (E2P4). O estresse de contenção foi aplicado por 30 minutos entre 09:00h e 10:00h na fase do diestro, ou 20 dias após o início da terapia hormonal (grupos VCD+E2, VCD+P4 e VCD+E2P4), de 75 a 85 dias após o início da administração de VCD/Óleo. O sangue foi coletado imediatamente (0min) e 60min após o final do estresse, quando os animais foram anestesiados e perfundidos para obtenção do tecido cerebral e posterior estudo imunohistoquímico das áreas de interesse. As concentrações basais de corticosterona foram semelhantes entre os grupos Óleo e VCD não estressadas. Contudo, asecreção de corticosterona em resposta ao estresse das ratas em periestropausa foi 72% menor que a do grupo controle. As concentrações basais de progesterona das ratas em periestropausa foram menores do que aquelas das ratas controles, mas o aumento da secreção deste hormônio induzido pelo estresse agudo por contenção não foi diferente entre os grupos. Centralmente, nas subdivisões PaMP e PaPo do PVN, assim como no LC, o número de neurônios c-Fos positivos expressos não foi diferente entre ratas VCD e óleo e o estresse aumentou de maneira semelhante o número de neurônios ativados em ambos os grupos. A secreção de corticosterona de animais em periestropausa tratados com estradiol, associado ou não à progesterona, foi ainda mais atenuada. Por outro lado, nas ratas tratadas com progesterona, as concentrações de corticosterona após o estresse mostraram-se mais elevadas que as do grupo VCD estressado sem tratamento hormonal. Todos os grupos tratados com hormônios aumentaram a secreção de progesterona em resposta ao estresse, no entanto esta resposta foi amplificada pelo estradiol. Nenhum dos tratamentos hormonais modificou a atividade neuronial após o estresse na PaMP, embora todos tenham atenuado esta resposta na PaPo. No LC, todos os tratamentos bloquearam o aumento de atividade neuronial induzida pelo estresse. Uma hora após o final do estresse, as concentrações de corticosterona e progesterona retornaram aos níveis basais observados nas ratas não estressadas. No entanto, nos grupos tratados com estradiol, os níveis de progesterona não retornaram aos basais, sendo estes níveis significantemente maiores após o fim do estímulo. Em conjunto, nossos resultados demonstram que na periestropausa, embora a secreção de progesterona em resposta ao estresse esteja preservada, a capacidade da adrenal em secretar corticosterona está reduzida. Esta redução parece não estar associada à deficiência central no funcionamento do eixo HPA (PVN) ou do sistema simpático central (LC), mas sim, a disfunções na esteroidogênese adrenal, que foram parcialmente corrigidas pela progesterona exógena. A diminuição da atividade neuronial do LC pelos esteróides ovarianos sugere uma possível atenuação do tônus simpático por estes hormônios. Ainda, a capacidade de recuperação pós-estresse da secreção de corticosterona e de progesterona se mostrou preservada neste modelo experimental.Perimenopause is characterized as the period of transition from reproductive to nonreproductive life in women, and begins with the onset of clinical symptoms, lasting up to one year after the last menstrual period. This phase is characterized by irregular menstrual cycles, alterations in hormonal production, as well as by behavioral, neuroendocrine and metabolic changes, and increased vulnerability to affective disorders when compared to other phases of life. Despite the various studies on the manifestations of these symptoms during perimenopause, little is known about the changes in hypothalamic-pituitary-adrenal (HPA) axis activity and the response to stress. The chemical reagent diepoxide 4-vinylcyclohexene (VCD) accelerates the natural process of follicular atresia, enabling studies of this phase of reproductive life. Therefore, its application in rodents constitutes an excellent experimental model capable of simulating in animals what occurs during perimenopause. Thus, the objective of this study was to evaluate, in an animal model of perimenopause: 1) the endocrine responses (corticosterone and progesterone) as well as the neuronal response (parvocellular subdivisions of PVN, medial- PaMP) and posterior-PaPO and locus coeruleus - LC) to restraint stress and 2) the influence of hormonal therapy on these responses. Female Wistar rats received subcutaneous injections of Oil or VCD for 15 consecutive days, from the 28th day of life. Around the 56th to 66th day of the onset of Oil or VCD administration, the rats of the groups to be stressed received subcutaneous implants of a pellet containing placebo (PL), estradiol (E2), progesterone (P4) or estradiol + progesterone (E2P4 ). Restraint stress was applied for 30 minutes between 09:00 and 10:00 in the diestrus phase, or 20 days after the onset of hormonal therapy (VCD + E2, VCD + P4 and VCD + E2P4 groups), from 75 to 85 days after starting VCD / Oil administration. The blood was collected immediately (0min) and 60min after the end of stress, when the animals were anesthetized and perfused to take the brain for immunohistochemistry of PVN and LC. Basal corticosterone concentrations were similar between the non-stressed Oil and VCD groups. However, corticosterone secretion in response to stress was 72% lower than that of the control group. The basal progesterone concentrations of periestropausal rats were lower than those of the control rats, but the increase in the secretion of this hormone induced by stress was not different between thegroups. Centrally, in the PaMP and PaPO subdivisions of PVN as well as LC, the number of c-Fos positive neurons expressed was not different between VCD and Oil rats and the stress increased similarly the number of activated neurons in both groups. Corticosterone secretion from estradiol-treated periestropause rats, associated or not with progesterone, was further attenuated. On the other hand, in rats treated with progesterone, post-stress corticosterone concentrations were higher than those in the stressed VCD group without hormonal treatment. All groups treated with hormones increased progesterone secretion in response to stress, however this response was amplified by estradiol. None of the hormone treatments modified neuronal activity after stress in PaMP, although all hormone treatment attenuated this response in PaPo. In the LC, all treatments blocked the increase of neuronal activity induced by stress. One hour after the end of stress, corticosterone and progesterone concentrations returned to the baseline levels observed in the non-stressed rats. However, in the estradioltreated groups, progesterone levels did not return to the basal levels, these levels being significantly higher after the end of the stimulus. Taken together, our results demonstrate that in periestropause, although progesterone secretion in response to stress is preserved, the ability of the adrenal to secrete corticosterone is reduced. This reduction appears not to be associated with a central deficiency in HPA axis (PVN) or central sympathetic (LC) function, but rather to dysfunctions in adrenal steroidogenesis, which have been partially corrected by exogenous progesterone. The reduction of neuronal LC activity by ovarian steroids suggests a possible attenuation of sympathetic tone by these hormones. Furthermore, the post-stress recovery capacity of corticosterone and progesterone secretion seems to be preserved in this experimental model.
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Cruickshank, Nicholas Christopher. "The Effects Of Hypothalamic Brain-Derived Neurotrophic Factor On Catecholaminergic Regulation Of Cardiovascular Function." ScholarWorks @ UVM, 2017. http://scholarworks.uvm.edu/graddis/804.
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Considerable evidence supports the claim that a hyperactive sympathetic nervous system (SNS) is involved in most cases of human hypertension, and therefore a more thorough understanding of the central regulation of the SNS may help elucidate novel therapeutic options. The PVN is a key region in SNS regulation of blood pressure (BP) and heart rate (HR). Stimulation of the parvocellular PVN neurons has been shown to enhance sympathetic outflow and thereby increase BP. Brain-derived neurotrophic factor (BDNF), a modulator of neuronal activity is upregulated in the paraventricular nucleus of the hypothalamus (PVN) in response to several hypertensive stimuli such as stress and hyperosmolarity, and previous studies from our lab demonstrated that both acute injections or chronic overexpression of BDNF in the PVN elevate SNS activity and BP. However, the BDNF-mediated hypertensive mechanisms are not completely understood. PVN neurons are under tonic inhibition from NTS catecholaminergic projections under baseline condition as indicated by significant BP increase after selective lesioning of NTS NE-ergic neurons. In addition, BDNF has been shown to alter NE-ergic signaling in multiple brain regions raising the possibility that BDNF may increase SNS activity and BP by interfering with NE-ergic inhibition of PVN sympathoregulatory neurons. Therefore, we tested the hypothesis that BDNF increases SNS activity and BP in part by disabling inhibitory actions of NTS catecholaminergic projections to the PVN by altering the expression of adrenergic receptors and NET in the PVN.
First, blood pressure was recorded using radiotelemetry in male Sprague-Dawley rats following bilateral microinjections of adeno-associated viral vectors expressing green fluorescent protein (GFP) or myc-tagged BDNF in the PVN and microinjections of phosphate saline buffer (PBS) or Anti-Dopaine Beta Hydroxylase (DBH)-conjugated saporin (DSAP), a catecholaminergic neuron-specific neurotoxin, into the NTS. Blood pressure was monitored both during resting conditions and during acute stress tests. A second group of rats received bilateral microinjections of adeno-associated viral vectors expressing GFP or myc-tagged BDNF in the PVN, and were sacrificed after 5 weeks. PVN and NTS samples were then selectively isolated using a brain punch tool, and expression of TH, DBH, 1a, 1b, 2a, 1, 2 receptors, and norepinephrine transporter (NET) was analyzed using quantitative RT-PCR.
Our results show that BDNF overexpression in the PVN leads to increased expression of catecholamine synthesizing enzymes in the NTS. In addition, both BDNF overexpression in the PVN, and DSAP lesioning in the NTS increased MAP compared to control rats. However, combined treatment with BDNF and DSAP failed to have any additional hypertensive effects suggesting that BDNF treatment may abolish the inhibitory effect of NTS catecholaminergic projections. Lesioning the NTS catecholaminergic neurons didn’t appear to have a significant effect on mean arterial pressure response to the stress tests, although DSAP treatment appeared to decrease the initial heart rate response to acute stress, and this effect was most pronounced in GFP rats. These results indicate that BDNF overexpression in the PVN desensitizes sympathoregulatory neurons to inhibitory NTS catecholaminergic projections during baseline conditions.
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Martinetz, Stefanie [Verfasser], and Inga D. [Akademischer Betreuer] Neumann. "Molecular underpinnings of anxiety regulation: Novel insights into the role of the purinergic and oxytocinergic systems within the paraventricular nucleus of the hypothalamus / Stefanie Martinetz. Betreuer: Inga D. Neumann." Regensburg : Universitätsbibliothek Regensburg, 2014. http://d-nb.info/1059004623/34.
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Neto, Hildebrando Candido Ferreira. "Estudo da interação entre ATP e glutamato em neurônios do núcleo paraventricular do hipotálamo e sua relação com a resposta simpatoexcitatória induzida por alterações na osmolaridade." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-19022015-143700/.
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Neste trabalho investigamos a interação entre ATP-glutamato na modulação de potenciais de ação e atividade sináptica de neurônios PVN-RVLM, além de avaliar se esta interação induziria mudanças na atividade simpática lombar (ANSL) por estímulo osmótico. Utilizamos de técnicas de imunohistoquímica, whole-cell patch clamp e registro eletroneurográfico. Observou-se que o ATP aumenta a frequência de potenciais de ação em neurônios PVN-RVLM, efeito bloqueado por acido quinurênico (KYN) e PPADS. A injeção de ATP no PVN aumenta a ANSL (25 nmol: 72%), um efeito atenuado por PPADS e/ou KYN, e também por CNQX. O ATP não afeta a função sináptica, mas aumenta correntes glutamatérgicas induzidas por aplicação AMPA em 52%, a qual foi bloqueada por PPADS ou por quelação de Ca2+ intracelular. Além disso, o estímulo osmótico ativa neurônios do PVN que expressam receptores P2X2 e potencia as correntes mediadas por AMPA (53%), um efeito bloqueado por PPADS. Finalmente, demonstrou-se que receptores P2 no PVN são importantes na simpatoexcitação induzida por estímulo osmótico agudo.In the present study we investigate the interaction of ATP-glutamate on the firing activity and synaptic function in PVN-RVLM neurons, besides whether that interaction would be translated in changes on sympathetic nerve activity (SNA) induced by osmotic stimulus. Immunohistochemistry, whole-cell patch clamp and electroneurography technical approaches were used. Our data have shown that ATP increases firing rate of PVN-RVLM neurons, an effect blocked by kynurenic acid (KYN) or PPADS. ATP injection into the PVN enhanced SNA (72%), which was attenuated by PPADS and/or KYN, or CNQX. ATP did not affect synaptic function but, glutamatergic currents evoked by AMPA application were augmented with ATP (AMPA area: 52%), blocked by PPADS and chelation of intracellular Ca2+. In addition, we observed that acute osmotic stimulus activates P2X2 expressing neurons in the PVN. Moreover, an osmotic challenge potentiated AMPA responses (53%), an effect blocked by PPADS. Finally, we demonstrated that P2 receptors in the PVN are important for osmotically-driven sympathoexcitation.
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Masson, Gustavo Santos. "Treinamento aeróbio x disfunção autonômica na hipertensão espontânea: uma abordagem molecular em núcleos centrais de regulação." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/42/42137/tde-19112014-133201/.
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Disfunção autonômica, inflamação e estresse oxidativo são características da hipertensão. Investigamos a cronologia das adaptações fisiológicas e celulares induzidas pelo treinamento aeróbio em ratos espontaneamente hipertensos (SHR). SHR exibiam disfunção autonômica e, no núcleo Paraventricular no hipotálamo (PVN), estresse oxidativo e inflamação. Duas semanas de treinamento aeróbio normalizaram a função autonômica, estresse oxidativo, inflamação, ativação de microglia e conteúdo de HMGB no PVN. Após 8 semanas, SHR treinados apresentaram menor pressão arterial e resistência vascular periférica. Redução do conteúdo de HMGB1 consiste num mecanismo para explicar os benefícios do treinamento, já que infusão aguda intracerebroventricular de HMGB1 produziu disfunção autonômica e ativação de microglia pela sinalização do CxCr4. Assim, redução do estresse oxidativo e da inflamação induzida pelo treinamento contribui para a reversão da disfunção autonômica na hipertensão e a redução da liberação de HMGB1 explica estes benefícios.Autonomic dysfunction, inflammation and oxidative stress are hallmarks in hypertension. We evaluated time-course of physiologic and cellular adaptations induced by aerobic training in spontaneous hypertensive rat (SHR). SHR showed autonomic dysfunction and, in the hypothalamic paraventricular nucleus (PVN), oxidative stress and inflammation. 2-weeks of aerobic training normalized autonomic function, oxidative stress, inflammation, microglia activation and HMGB1 content into the PVN. After 8-weeks, trained SHR exhibited lower arterial pressure and peripheral vascular resistance. Decrease of HMGB1 content is a mechanism to explain these training benefits, since HMGB1 intracerebroventricular acute infusion induced autonomic dysfunction, microglia activation through CxCr4 signaling. So, decrease of oxidative stress and inflammation induced by aerobic training contributes to reverse autonomic dysfunction in hypertension and decrease of HMGB1 content explains these benefits.
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Foster, Michelle Tranace. "Central Nervous System Regulation of Fat Cell Lipid Mobilization: The Role of the Sympathetic Nervous System." Digital Archive @ GSU, 2006. http://digitalarchive.gsu.edu/biology_diss/2.
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Obesity is a growing disorder in the United States, affecting over 60% of the population. We previously defined sympathetic nervous system (SNS) outflow from brain to white adipose tissue (WAT) using a viral transneuronal tract tracer. SNS innervation of WAT is the principle initiator of lipolysis, whereas decreases in sympathetic drive promote lipid accumulation. Which of the many origins of SNS outflow from brain to WAT results in SNS-mediated changes in lipid mobilization (increases in drive) or accumulation (decrease in drive) is unknown. Previous research indicates that sympathetic denervation blocks lipid mobilization; thus, rostral sites in the neuroaxis connected to WAT via the SNS may promote WAT lipid mobilization. The hypothalamic paraventricular nucleus (PVN) may play a role via its descending projections to the intermediolateral horn of the spinal cord. Therefore, the consequences of PVN lesions (PVNx) on WAT mobilization or accumulation were tested. PVNx resulted in increased lipid accumulation, indicated by increases in retroperitoneal (RWAT) , epididymal (EWAT) , and inguinal WAT (IWAT) pad masses, in fed hamsters, but PVNx did not block fasting (56 h)-induced lipid mobilization. Because adrenal medullary catecholamines, especially epinephrine, also play a minor role in lipid mobilization, we tested the contribution of catecholamine release on lipid mobilization through adrenal demedullation (ADMEDx), with and without PVNx, and found fastinginduced lipid mobilization was not blocked. There was, however, a suggestion that distal denervation of IWAT, with and without ADMEDx, partially blocked lipid mobilization. In addition, evidence suggests SNS also may be an important controller of fat cell proliferation. Surgical denervation of WAT triggers increases in fat cell number (FCN), but have not determined if this FCN increase is due to preadipocyte proliferation or differentiation of preadipocytes into mature fat cells. We also have not demonstrated what role sensory innervation may have in regulating white adipocyte proliferation. Therefore, the role of WAT sympathetic or sensory innervation on adipocyte proliferation was tested. The SNS but not sensory denervation triggered bona fide proliferation as indicated by bromodeoxyuridine plus AD3, a specific adipocyte membrane protein, colabeling. These and previous data suggest that the SNS plays a role in regulating adiposity.
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VAN, HOOREN DANIELLA CHRISTINE. "GluR5 IS INVOLVED IN REGULATION OF THE HPA AXIS." University of Cincinnati / OhioLINK, 2004. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1080156678.
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Maken, Deborah Suzanne. "Central Mechanisms Regulating Pituitary-Adrenal Activity in Infant Guinea Pigs (Cavia porcellus) during Exposure to Psychological Stressors: Independent and Combined Effects of Maternal Separation and Novelty." Wright State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=wright1259610672.
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Gannon, Sean Michael. "Plasticity in the intermediolateral cell column of the spinal cord following injury to sympathetic postganglionic axons." Miami University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=miami1407112137.
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Pingili, Ajeeth Kumar. "Augmented Expression of Apelin/APJ in the Paraventricular Nuclei of Rats after Myocardial Infarction." Diss., North Dakota State University, 2012. https://hdl.handle.net/10365/26749.
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Heart failure (HF) is a disease condition in which insufficient blood is pumped through the body. The pathophysiology of HF is multisystematic and includes a collection of different responses to compensate for the inability of the heart to pump the blood with the most important outcome being increased sympathetic nervous system (SNS) activity. Increased SNS activity leads to reclaim the reserved cardiac function. However, this adaptive response is short term and deleterious. The central mechanisms that lead to increased SNS activity during conditions of HF remain enigmatic. APJ, a G-protein-coupled receptor and its endogenous ligand, is a novel neuroendocrine system. Previous studies from us and others indicated that central administration or over expression of apelin in brain cardiovascular regulatory areas resulted in an increase in blood pressure, sympathetic nerve activity and cardiac hypertrophy. The main objective of this study is to determine whether the Apelin/APJ system is involved in increased SNS activation during HF. We created HF rat models by left coronary artery ligation. Apelin and APJ receptor mRNA levels were measured in cardiovascular regions of the brain of sham and myocardial infarction (MI) rats. Results showed a significant increase in the levels of Apelin/APJ mRNA levels in paraventricular nuclei (PVN) and rostral ventrolateral medulla (RVLM) in MI rats as compared to sham rats. To determine the functional role of elevated APJ receptor in these cardiovascular regulatory regions of the brain during HF, we constructed a lentiviral vector carrying an APJ shRNA (Lenti-APJ-shRNA) to knockdown the APJ receptor. Efficiency of the lentiviral vector to knockdown the APJ receptor was confirmed in vitro by transducing a Cath.a cell line and a primary neuronal cell culture with Lenti-APJ-shRNA. In order to determine the effect of silencing of the APJ receptor in vivo, Lenti-APJ-shRNA virus was injected into the PVN of the MI and sham rats. Results showed knockdown of APJ receptor improved left ventricular function and decreased myocardial fibrosis and hypertrophy in MI rats. Thus, this study shows that PVN plays an important role in sympatho excitation and pathophysiology of HF and these findings may help in developing effective therapies for HF.
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Juss, T. S. "Reflex pathways controlling oxytocin cells in the supraoptic and paraventricular nuclei during suckling in the rat." Thesis, University of Bristol, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379546.
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Czell, David. "Die Wirkung intrathekaler Baclofenapplikation auf die Freisetzung von Adrenalin, Noradrenalin und Homovanillinsäure aus dem Nucleus paraventricularis hypothalami der Ratte." [S.l.] : [s.n.], 2003. http://archiv.ub.uni-marburg.de/diss/z2003/0720/.
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McKinnon, Mark S. (Mark Steven). "The Effect of Long-Term Moderate Amounts of Ethanol on Paraventricular Nuclei Activity on Cold Stressed Adult Rats." Thesis, University of North Texas, 1990. https://digital.library.unt.edu/ark:/67531/metadc500872/.
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The effects of moderate, long-term intake of ethanol on the hypothalamic response to cold stress were examined. The long-term experimental animals were given .25 ml of 28% ethanol or .25 ml of water orally once a day, five days a week for fourteen months. A stainless steel electrode was then surgically implanted into the paraventricular nucleus, after which the animal was subjected to cold stress (-150 C, 10 min.). Recordings were taken in the forms of frequency and activity. The data clearly indicate that: (1) alcohol fed rats exhibited a suppressed response to cold stress compared to sham-fed rats; (2) this suppression of activity occurred at the level of the hypothalamus, and (3) mortality was significantly lower in alcohol-fed males than it was in sham fed males. This study clearly points out the need for further work in the area of the beneficial effects of moderate doses of alcohol.
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Dreesen, Anna Frieda Maria [Verfasser], and Kay [Akademischer Betreuer] Jüngling. "Modulation neuronaler Aktivität durch Neuropeptid S im Nucleus paraventricularis anterior thalami der Maus / Anna Frieda Maria Dreesen ; Betreuer: Kay Jüngling." Münster : Universitäts- und Landesbibliothek Münster, 2019. http://d-nb.info/1183096208/34.
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Peter, Lisa [Verfasser]. "Peripher injiziertes sulfatiertes Cholezystokinin-Oktapeptid aktiviert Cocaine- and amphetamine-regulated transcript-immunreaktive Neurone des Nucleus paraventricularis in Ratten / Lisa Peter." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2014. http://d-nb.info/1062536959/34.
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Collares-Buzato, Carla Beatriz 1965. "Estudo sobre o efeito do estresse no esvaziamento gastrico de liquidos em ratos : envolvimento do nucleo paraventricular do hipotalamo." [s.n.], 1991. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314257.
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Orientador: Gilberto D'Assunção FernandesDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-07-13T23:39:03Z (GMT). No. of bitstreams: 1 Collares-Buzato_CarlaBeatriz_M.pdf: 3582256 bytes, checksum: 3f6c61dc70a6c0d3f5fa1836ec2b4925 (MD5) Previous issue date: 1991
Resumo: o presente trabalho teve como objetivos: 1) propor um modelo experimental adequado para o estudo do efeito do estresse sobre o esvaziamento gástrico (EG); 2) verificar os possíveis componentes (secreção ácida e/ou motilidade gástrica) implicados na alteração do EG induzida pelo estresse e 3) investigar o provável envolvimento vagal e do núcleo hipotâmico paraventricular sobre o processo. Para tal, este estudo foi conduzido em 3 etapas, utilizando-se um total de 322 ratos Wistar machos. Na Etapa 1, os animais foram submetidos ao estresse de contenção ou contenção a frio (4°C) durante o teste de EG de um solução de glicose 5 %. Foi feita também a dosagem por radioimunoensaio de corticosterona sérica em um grupo paralelo de animais sujeitos ou não à contenção a frio. Na Etapa 2, executou-se em ambos grupos, Controle e Estressado (contenção a frio), o teste de EG com uma solução de bicarbonato 0,25 M (aos 10 min) ou pré-tratamento com cimetidina (10 e 50 mg/kg/1h, ip) e posterior avaliação do esvaziamento de glicose (aos 30 min) ou bicarbonato (10 min). Por fim, na Etapa 3, os ratos controles e estressados (contenção a frio) foram submetidos à cirurgia de vagotomia sub-diafragmática ou lesão eletrolíticabilateral do NPV, 15 dias antes do teste do EG com glicose 5 %(aos 30 min). o EG foi avaliado medindo-se a retenção gatrica (RG) da refeição de prova. Para tal, os animais receberam por via orogástrica, através de uma sonda metálica, a solução teste (2 ml/100g de peso do animal), na qual foi adicionado o marcador fenolsulfonftaleína (6 mg/1O0ml de solução). A RG foi determinada calculando-se a quantidade do marcador retido no resíduo gástrico, após determinado tempo. Em todas as etapas executadas, os animais pertencentes ao grupo Estressado foram sujeitos ao estresse durante esse processo. O estresse de .contenção não induziu alteração da RG de glicose avaliada aos 30 min, enquanto que os animais sob contenção a frio apresentaram um retarde do EG dessa solução, não significante aos 10 min, mas estatisticamente significativo aos 20 e 30 min da avaliação. O estresse de contenção a frio, durante 30 min, mostrou-se igualmente efetivo em induzir aumento do nível de corticosterona no soro. Adicionalmente, sob contenção a frio, os animais mostraram EG mais rápido de bicarbonato, que foi bloqueado por ambas as doses (10 e 50 mg/kg) de cimetidina. Entretanto, o aumento da RG de glicose foi somente inibido pela maior dose testada dessa droga (50 mg/kg). Ainda, na dose de 50 mg/kg, a cimetidina induziu per se retarde do EG de ambas as refeições de prova nos animais controles. O EG de bicarbonato constitui-se num índice indireto da secreção de HCI pelo estômago, pois encontra-se acelerado em situações de hipersecreção ácida. Sendo assim nossos dados indicam um aumento de secreção gástrica de ácido pelos animais estressados. Entretanto, os resultados obtidos ainda não foram suficientes para se apontar conclusivamente a real importância da secreção ácida na determinação do retarde do EG de glicose, provocada pelo estresse. Finalmente, tanto a secção do nervo vago como a lesão do NPV bloquearam totalmente o aumento da RG de glicose observado nos animais estressados não submetidos a essas intervenções cirúrgicas. Portanto, possivelmente, este núcleo hipotalâmico, através de vias eferentes vagais, medeia essa alteração gastrointestinal resultante do estresse
Abstract: The objects of the present study were: 1) to examine the effect of restraint and cold-restraint stress on gastric emptying of a liquid test meal; 2) to establish the role of gastric acid secretion in the genesis of the stress-induced alteration of gastric emptying and 3) to verify the involvement of the vagal nerve and hypothalamic paraventricular nucleus upon this alteration. The gastric emptying was evaluated by measuring the gastric retention of a test me aI. Male Wistar rats received an orogastric infusion, through a stainless steel tube, of the test me aI (2 ml/1O0 g body weight) containing phenol red (6 ml/1O0 ml) as a marker. Gastric retention was determined by measuring the concentration of the marker in the residual test meal recovered from the stomach after killing the animal. In a first series of experiments, the animaIs were submitted to restraint or coldrestraint (40C) stress soon after the injection of a test meal which consisted of a solution of 5 %glucose. The control group was replaced in the individual cages at room temperature after administration of the test meal. The serum levels of corticosterone were also determined in blood samples obtained by decapitation of other control and stressed (cold-restraint) rats. In a second series of experiments, gastric retention of a solution of sodium bicarbonate 0,25 M was evaluated in both control and stressed (cold-restraint) groups. Additionally, stressed and nonstressed animaIs were pretreated with cimetidine (10 and 50 mg/kg body weight); subsequently, gastric retention of 5 %glucose or 0,25 M bicarbonate was determined. FinaIly, in a third series of experiments, truncal vagotomy or bilateral electrolytic lesion of the hypothalamic paraventricular nucleus (PVN) were performed previously (15 days before), after which gastric retention of 5 %glucose was studied in control and stressed (cold-restraint) groups. Restraint stress did not induce changes in gastric retention of glucose at 30 min; however, cold-restraint stress significantly delayed gastric emptying of this solution at 20 and 30 mino The animaIs subjected to cold-restraint for 30 min also showed a rise in serum corticosterone compared to the control animaIs. In addition, under cold-restraint stress, the gastric emptying of bicarbonate was faster than in control conditions. This gastric alteration was significantly blocked by pretreatment with two doses (10 and 50 mg/kg) of cimetidine, a well-known antisecretory agent. Meanwhile, the increase in the gastric retention of glucose after cold-restraint exposure was only inhibited by 50 mg/kg dose of this drug. Cimetidine, in this dose (50 mg/kg), also induced per se delay of the gastric emptying of both test meals in the control rats. As described in the literature, the gastric emptying of a bicarbonate solution is accelerated when there is a rise in the acid secretion by the gastric mucosa. Thus,our findings indicate that in stressed animaIs a gastric acid hypersecretion is found. On the other hand, the results of pretreatment with cimetidine are insufficient to determine the importance of gastric acid as a factor in the stress-induced change on gastric emptying of glucose. Finally, both truncal vagotomy and PVN lesion completely blocked the cold-restraint -induced delay of gastric emptying of the glucose solution. These data, therefore, suggest an important role for PVN efferents, probably infiuencing medullary vagal preganglionic neurons, in the development of this gastric alteration during stress condition
Mestrado
Fisiologia
Mestre em Ciências Biológicas
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Czell, David [Verfasser]. "Die Wirkung intrathekaler Baclofenapplikation auf die Aussschüttung von Adrenalin, Noradrenalin und Homovanillinsäure aus dem Nucleus paraventricularis hypothalami der Ratte / David Czell." München : GRIN Verlag, 2004. http://d-nb.info/1082043079/34.
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Popeski, Naomi. "NADPH-d staining in the supraoptic and paraventricular nuclei increases in late pregnant and lactating rats and is influenced by ovarian steroids and central oxytocin levels." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ40185.pdf.
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McGlashan, Megan. "Relaxin and the Paraventricular Nucleus of the Hypothalamus." Thesis, 2013. http://hdl.handle.net/10214/7386.
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The hormone relaxin regulates the release of the magnocellular hormones, oxytocin and vasopressin, from the central nervous system. Studies have yet to determine whether relaxin regulates magnocellular hormone release through the circumventricular organs alone, or whether relaxin can act on the brain regions containing the magnocellular neurons as well. The paraventricular nucleus of the hypothalamus was isolated from other brain regions and maintained in vitro, in order evaluate the effects of the relaxin and relaxin-3 on the somatodendritic release of oxytocin and vasopressin. At 50 nM concentrations, relaxin induced oxytocin release, while relaxin-3 inhibited oxytocin release. Neither relaxin nor relaxin-3 had an effect on the vasopressin release, however the RXFP3 specific agonist, R3/I5, induced vasopressin release. The effect of the relaxin peptides on the electrical activity of neurons in the paraventricular nucleus was also evaluated. Relaxin depolarized magnocellular neurons while relaxin-3 hyperpolarized the neurons. Relaxin and relaxin-3 appear to have differential effects on the magnocellular neurons of the paraventricular nucleus.
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Khademullah, CHARLINE SAHARA. "HYDROGEN SULFIDES ACTIONS IN THE PARAVENTRICULAR NUCLEUS OF THE HYPOTHALAMUS." Thesis, 2013. http://hdl.handle.net/1974/8293.
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Hydrogen sulfide (H2S) is a novel neurotransmitter that has been shown to influence cardiovascular function as well as other autonomic and endocrine functions by targeting a wide range of ion channels. Using whole-cell electrophysiology, I have investigated the potential role of H2S in the regulation of neuronal excitability in the paraventricular nucleus of the hypothalamus (PVN), which is a central relay centre for autonomic and endocrine function.
In current-clamp recordings, sodium hydrosulfide hydrate (NaHS), when perfused onto PVN slices at various concentrations (0.1, 1, 10, and 50 mM), elicited a concentration-dependent response relationship from the majority of recorded neurons, with almost exclusively depolarizing effects. Input resistance differences from baseline, and during the NaHS-induced depolarization, uncovered a biphasic response, implicating both a potassium (K+) and non-selective cation conductance.
In order to further investigate H2Ss effects on K+ conductances, we used both voltage- and current-clamp techniques to examine the effects of NaHS at either 1 or 10 mM on both the transient and sustained voltage-activated K+ currents in these neurons. We applied TEA+ (10 mM) to isolate the transient/rapidly inactivating current (IA) and 4-AP (5 mM) to isolate the sustained/delayed rectifier current (IK), and were able to show that both of these conductances were significantly reduced by H2S. Finally, we were able to demonstrate, using current-clamp, that when 4-AP and TEA+ were applied together with NaHS, they were able to completely eliminate the previously observed NaHS-induced depolarization, and the effects on membrane potential reversed to show a small hyperpolarization.
These data highlight the potential role of H2S as a critical modulator of the voltage-gated repolarizing conductances, IA and IK, which in turn regulate neuronal excitability within the PVN. This can have a large impact on the way neurotransmitters and hormones such as vasopressin, oxytocin, corticotrophin-releasing hormone, and thyrotrophin-releasing hormone are released from the PVN, which influence a wide range of neuroendocrine and autonomic functions such as cardiovascular function, fluid balance, and food intake.Thesis (Master, Neuroscience Studies) -- Queen's University, 2013-09-13 10:51:34.585