Relevant bibliographies by topics / Hypothalamus

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Hypothalamus'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 June 2025

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Journal articles on the topic "Hypothalamus"

1

Hagan, P., S. Poole та A. F. Bristow. "Endotoxin-stimulated production of rat hypothalamic interleukin-1β in vivo and in vitro, measured by specific immunoradiometric assay". Journal of Molecular Endocrinology 11, № 1 (1993): 31–36. http://dx.doi.org/10.1677/jme.0.0110031.

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ABSTRACT Regulation of a number of aspects of the acute-phase response, including induction of fever and activation of the hypothalamo-pituitary-adrenal axis, occurs within the hypothalamus. The acute-phase response appears to be co-ordinated by the inflammatory cytokine interleukin-1 (IL-1). A number of studies using hybridization techniques to measure IL-1 gene expression and immunocyto-chemistry to localize immunoactive IL-1 have established the concept that the central nervous system, and in particular the hypothalamus, is a site of IL-1 production, and that levels increase in response to inflammatory stimuli. In this report we present data on the levels of IL-1β produced in the rat hypothalamus using quantitative immunoassay techniques. Bacterial endotoxin, administered to rats in vivo, evoked increases in hypothalamic IL-1β levels which were significant within 1 h, and reached maximum levels at 5–10 h. The response to endotoxin was dose-related, and levels reached in hypothalamic extracts corresponded to intra-hypothalamic levels of the order of 20 ng/ml. During short-term in-vitro culture of rat hypothalami, endotoxin stimulated a dose-related increase in both the synthesis and the secretion of IL-1β, which reached similar levels to those seen after in-vivo stimulation. Hypothalami obtained from animals stimulated with endotoxin in vivo did not, however, show any evidence of persistent stimulation of IL-1β production when subsequently cultured in vitro. These data support the concept that production of hypothalamic IL-1 is an essential step in regulating the activity of the hypothalamus during the acute-phase response, and provide for the first time quantitative data on the magnitude, dose—response relationships and time-courses of rat hypothalamic IL-1β production in vivo and in vitro.
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KUNPASURUANG, WANNAPA, YONGWIMON LENBURY, and GEERTJE HEK. "A NONLINEAR MATHEMATICAL MODEL FOR PULSATILE DISCHARGES OF LUTEINIZING HORMONE MEDIATED BY HYPOTHALAMIC AND EXTRA-HYPOTHALAMIC PATHWAYS." Mathematical Models and Methods in Applied Sciences 12, no. 05 (2002): 607–24. http://dx.doi.org/10.1142/s0218202502001817.

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A mathematical model of hormone secretion in the hypothalamo-pituitary-gonadal axis in man is extended to incorporate two different neural pathways, which have been suggested by clinical data to be capable of stimulating pulsatile discharges of LH (luteinizing hormone) independently of each other. Analysis of the nonlinear model is carried out through the use of geometric singular perturbation methods. In this way, existence of a limit cycle is proved for certain ranges of the system parameters. When the LH secretion rate independent of the hypothalamus is assumed constant, dropping the hypothalamus stimulated secretion term from the model blocks the hypothalamus pathway, implying that sustained oscillations in the hormone levels may not be attainable. Therefore, a sinusoidal term is incorporated into the model so that the system can still exhibit pulsatile LH secretion independent of the hypothalamus mediation. It is shown, by a construction of a bifurcation diagram, that the pulsatile hormone secretion can develop into chaotic dynamics when the amplitude of oscillation stimulated by extra-hypothalamic structures is high enough to disturb the synchrony of hypothalamic control. The resulting numerical simulation is found to compare well with the clinically observed data.
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Khuroo, Z. B. "Cyclic Changes In The Hypothalamo Neurohypophysial System of Xenentodon Cancila (HAM.)." Indian Journal of Pharmaceutical and Biological Research 1, no. 02 (2013): 12–19. http://dx.doi.org/10.30750/ijpbr.1.2.3.

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The presence of functional hypothalamo-hypophysial neurosecretory system in vertebrates has led to revise earlier views regarding the hypothalamus-pituitary relationship. The hypothalamo-neurohypophysial system which consists of hypothalamic nuclei, their axonal fibres forming tractus preoptico-hypophyses and the neurohypophysis) works as a morphological as well as a physiological connection between the hypothalamus and the pituitary gland. In fishes, fibres from the neurosecretory hypothalamic nuclei terminate in the neurohypophysis, which remains inter digitized with the adenohypophysis and provides a very close association between the neurosecretory fibres and pars intermedia of the pituitary gland forming a neuro-intermediate lobe. Hypothalamo-Neurosecretory complex of Xenentodon cancila consists of Nucleus Pre-opticus (NPO), Nucleus Lateralis Tuberis (NLT) and their axonal tracts. NPO is a paired structure situated on either side of the third ventricle anterodorsal to the optic chiasma. NPO is divisible into a dorsal Pars Magnocellularis (PMC) consisting of large neurosecretory cells and Pars Parvocellularis (PPC) formed of smaller neurons. Neurons of PMC and PPC contribute beaded axons to form neurohypophysial tract. Herring bodies are seen in the anterior as well as posterior neurohypophysis.
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Gasparini, Silvia, Lauren M. Stein, Spencer P. Loewen, et al. "Novel regulator of vasopressin secretion: phoenixin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 314, no. 4 (2018): R623—R628. http://dx.doi.org/10.1152/ajpregu.00426.2017.

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The newly described hypothalamic peptide, phoenixin, is produced in the hypothalamus and adenohypophysis, where it acts to control reproductive hormone secretion. Both phoenixin and its receptor GPR173 are expressed in the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei, suggesting additional, nonreproductive effects of the peptide to control vasopressin (AVP) or oxytocin (OT) secretion. Hypothalamo-neurohypophysial explants released AVP but not OT in response to phoenixin. Intracerebroventricular administration of phoenixin into conscious, unrestrained male and female rats significantly increased circulating AVP, but not OT, levels in plasma, and it increased immediate early gene expression in the supraoptic nuclei of male rats. Bath application of phoenixin in hypothalamic slice preparations resulted in depolarization of PVN neurons, indicating a direct, neural action of phoenixin in the hypothalamus. Our results suggest that the newly described, hypothalamic peptide phoenixin, in addition to its effects on hypothalamic and pituitary mechanisms controlling reproduction, may contribute to the physiological mechanisms regulating fluid and electrolyte homeostasis.
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Ciechanowska, Magdalena, Magdalena Łapot, Tadeusz Malewski, Krystyna Mateusiak, Tomasz Misztal, and Franciszek Przekop. "Effects of corticotropin-releasing hormone and its antagonist on the gene expression of gonadotrophin-releasing hormone (GnRH) and GnRH receptor in the hypothalamus and anterior pituitary gland of follicular phase ewes." Reproduction, Fertility and Development 23, no. 6 (2011): 780. http://dx.doi.org/10.1071/rd10341.

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There is no information in the literature regarding the effect of corticotropin-releasing hormone (CRH) on genes encoding gonadotrophin-releasing hormone (GnRH) and the GnRH receptor (GnRHR) in the hypothalamus or on GnRHR gene expression in the pituitary gland in vivo. Thus, the aim of the present study was to investigate, in follicular phase ewes, the effects of prolonged, intermittent infusion of small doses of CRH or its antagonist (α-helical CRH 9-41; CRH-A) into the third cerebral ventricle on GnRH mRNA and GnRHR mRNA levels in the hypothalamo–pituitary unit and on LH secretion. Stimulation or inhibition of CRH receptors significantly decreased or increased GnRH gene expression in the hypothalamus, respectively, and led to different responses in GnRHR gene expression in discrete hypothalamic areas. For example, CRH increased GnRHR gene expression in the preoptic area, but decreased it in the hypothalamus/stalk median eminence and in the anterior pituitary gland. In addition, CRH decreased LH secretion. Blockade of CRH receptors had the opposite effect on GnRHR gene expression. The results suggest that activation of CRH receptors in the hypothalamus of follicular phase ewes can modulate the biosynthesis and release of GnRH through complex changes in the expression of GnRH and GnRHR genes in the hypothalamo–anterior pituitary unit.
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Yli-Mattila, Tapani, El-Refaie Kenawy, H. Rozsypal, et al. "An Overview of the Hypothalamus: A Review of Hypothalamic–Pituitary Axis and Autoantibody Related Disorders." Endocrinology and Disorders 1, no. 3 (2017): 01–03. http://dx.doi.org/10.31579/2640-1045/095.

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The hypothalamus is a portion of the brain that contains a number of small nuclei with a variety of functions. One of the most important functions of the hypothalamus is to link the nervous system to the endocrine system via the pituitary gland. The hypothalamus is located below the thalamus and is part of the limbic system. In the terminology of neuroanatomy, it forms the ventral part of the diencephalon. All vertebrate brains contain a hypothalamus. In humans, it is the size of an almond. The hypothalamus is responsible for the regulation of certain metabolic processes and other activities of the autonomic nervous system. It synthesizes and secretes certain neurohormones, called releasing hormones or hypothalamic hormones, and these in turn stimulate or inhibit the secretion of hormones from the pituitary gland.
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Aveleira, Célia A., Mariana Botelho, Sara Carmo-Silva, et al. "Neuropeptide Y stimulates autophagy in hypothalamic neurons." Proceedings of the National Academy of Sciences 112, no. 13 (2015): E1642—E1651. http://dx.doi.org/10.1073/pnas.1416609112.

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Aging is characterized by autophagy impairment that contributes to age-related disease aggravation. Moreover, it was described that the hypothalamus is a critical brain area for whole-body aging development and has impact on lifespan. Neuropeptide Y (NPY) is one of the major neuropeptides present in the hypothalamus, and it has been shown that, in aged animals, the hypothalamic NPY levels decrease. Because caloric restriction (CR) delays aging, at least in part, by stimulating autophagy, and also increases hypothalamic NPY levels, we hypothesized that NPY could have a relevant role on autophagy modulation in the hypothalamus. Therefore, the aim of this study was to investigate the role of NPY on autophagy in the hypothalamus. Using both hypothalamic neuronal in vitro models and mice overexpressing NPY in the hypothalamus, we observed that NPY stimulates autophagy in the hypothalamus. Mechanistically, in rodent hypothalamic neurons, NPY increases autophagy through the activation of NPY Y1 and Y5 receptors, and this effect is tightly associated with the concerted activation of PI3K, MEK/ERK, and PKA signaling pathways. Modulation of hypothalamic NPY levels may be considered a potential strategy to produce protective effects against hypothalamic impairments associated with age and to delay aging.
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Mathieu, Juliette, Anukampa Barth, Frederic M. Rosa, Stephen W. Wilson, and Nadine Peyriéras. "Distinct and cooperative roles for Nodal and Hedgehog signals during hypothalamic development." Development 129, no. 13 (2002): 3055–65. http://dx.doi.org/10.1242/dev.129.13.3055.

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Despite its evolutionary conservation and functional importance, little is known of the signaling pathways that underlie development of the hypothalamus. Although mutations affecting Nodal and Hedgehog signaling disrupt hypothalamic development, the time and site of action and the exact roles of these pathways remain very poorly understood. Unexpectedly, we show here that cell-autonomous reception of Nodal signals is neither required for the migration of hypothalamic precursors within the neural plate, nor for further development of the anterior-dorsal hypothalamus. Nodal signaling is, however, cell-autonomously required for establishment of the posterior-ventral hypothalamus. Conversely, Hedgehog signaling antagonizes the development of posterior-ventral hypothalamus, while promoting anterior-dorsal hypothalamic fates. Besides their distinct roles in the regionalization of the diencephalon, we reveal cooperation between Nodal and Hedgehog pathways in the maintenance of the anterior-dorsal hypothalamus. Finally we show that it is the prechordal plate and not the head endoderm that provides the early signals essential for establishment of the hypothalamus.
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Rawish, Elias, Laura Nickel, Franziska Schuster, et al. "Telmisartan prevents development of obesity and normalizes hypothalamic lipid droplets." Journal of Endocrinology 244, no. 1 (2020): 95–110. http://dx.doi.org/10.1530/joe-19-0319.

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The AT1 receptor blocker telmisartan (TEL) prevents diet-induced obesity. Hypothalamic lipid metabolism is functionally important for energy homeostasis, as a surplus of lipids induces an inflammatory response in the hypothalamus, thus promoting the development of central leptin resistance. However, it is unclear as to whether TEL treatment affects the lipid status in the hypothalamus. C57BL/6N mice were fed with chow (CONchow) or high-fat diet (CONHFD). HFD-fed mice were gavaged with TEL (8 mg/kg/day, 12 weeks, TELHFD). Mice were phenotyped regarding weight gain, energy homeostasis, and glucose control. Hypothalamic lipid droplets were analyzed by fluorescence microscopy. Lipidomics were assessed by performing liquid chromatography-mass spectrometry in plasma and hypothalami. Adipokines were investigated using immunosorbent assays. Glial fibrillary acidic protein (GFAP) was determined by Western blotting and immunohistochemical imaging. We found that body weight, energy homeostasis, and glucose control of TEL-treated mice remained normal while CONHFD became obese. Hypothalamic ceramide and triglyceride levels as well as alkyne oleate distribution were normalized in TELHFD. The lipid droplet signal in the tanycyte layer was higher in CONHFD than in CONchow and returned to normal under TELHFD conditions. High hypothalamic levels of GFAP protein indicate astrogliosis of CONHFD mice while normalized GFAP, TNFα, and IL1α levels of TELHFD mice suggest that TEL prevents hypothalamic inflammation. In conclusion, TEL has anti-obese efficacy and prevented lipid accumulation and lipotoxicity, which is accompanied by an anti-inflammatory effect in the murine hypothalamus. Our findings support the notion that a brain-related mechanism is involved in TEL-induced weight loss.
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Kim, Thomas. "Molecular Logic of Hypothalamus Development." Journal of the Endocrine Society 5, Supplement_1 (2021): A507. http://dx.doi.org/10.1210/jendso/bvab048.1037.

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Abstract The hypothalamus is a central regulator of physiological homeostasis. During development, multiple transcription factors coordinate the patterning and specification of hypothalamic nuclei. However, the molecular mechanisms controlling hypothalamic patterning and cell fate specification are poorly understood. To identify genes that control these processes, we have previously used single-cell RNA sequencing (scRNA-Seq) to profile mouse hypothalamic gene expression across multiple developmental time points and established database HyDD (Hypothalamus Developmental Database). We next used HyDD to characterize multiple mutant lines targetting key transcription factors that came out from our scRNA-Seq database (Nkx2.2, Dlx1/2, Isl1, Foxd1, Lhx2), and was able to comprehensively characterize mutants that have altered hypothalamic patterning. Our phenotype result supports a modified columnar model of organization for the diencephalon, where prethalamus and hypothalamus are situated in adjacent dorsal and ventral domains of the anterior diencephalon. Furthermore, using our mouse hypothalamus as a guideline, we are comparing scRNA-Seq dataset of developing chicken, zebrafish and human hypothalamus, to identify evolutionarily conserved and divergent region-specific gene regulatory networks. Lastly, we are improving mouse HyDD, in order to characterize adult hypothalamus neuronal subtypes.
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Dissertations / Theses on the topic "Hypothalamus"

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Bhumbra, Gardave Singh. "Coding in the hypothalamus." Thesis, University of Cambridge, 2004. https://www.repository.cam.ac.uk/handle/1810/251929.

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Fu, Sheung Ching. "Development of the chick hypothalamus." Thesis, University of Sheffield, 2016. http://etheses.whiterose.ac.uk/16313/.

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Sjoberg, Hanna. "Metabolic sensing in the hypothalamus." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/metabolic-sensing-in-the-hypothalamus(16aa8496-2f25-4967-be7a-fa0837b541b5).html.

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The hypothalamus is an established regulatory hub with regards to energy homeostasis. While the arcuate nucleus has been researched extensively and substantial emphasis has been put on its role in energy balance, the ventromedial nucleus of the hypothalamus (VMN) is still poorly understood. However, the anorexia-inducing pituitary adenylate-cyclase activating peptide (PACAP) and brain-derived neurotrophic factor (BDNF) have both been proposed as potential candidates as VMN-produced regulators. The mRNAs of both neuropeptides is up regulated in diet-induced obesity (DIO)-resistant mice, but not in DIO-prone mice, indicating that they could be responsible for signalling in the VMN, especially in terms of countering the effects of an obesogenic diet. The initial objective of this PhD project was to evaluate the effect of metabolic manipulation, in the form of fasting or feeding with high-energy diet (HED), on the gene expression of these two possible neuronal markers in the VMN. This was done using quantitative PCR and, while our findings did not fully support the hypothesis that PACAP and BDNF have protective roles against obesity, we determined that metabolic manipulation differentially regulates pacap and bdnf transcripts in the VMN of outbred mice. The presence of several bdnf transcripts in the VMN, and their differential regulation, indicates that the transcripts play distinct roles in the response to metabolic manipulation. The findings also added further support for the role of PACAP and BDNF as important signalling molecules in the VMN. Their identification as important cellular phenotypes, allows future manipulation of specific neurons in the VMN, which should help us to rapidly increase our knowledge of the nucleus and its functions. We utilised a transgenic mouse model where leptin receptor deletion is driven by pacap expression in PACAP—IRES-Cre recombinase mice, to study whether leptin is having a physiological role through PACAP neurons. However, since we may not have achieved full expression of cre recombinase in all PACAP neurons, it was difficult to interpret our results, leaving open the question of what is the role of PACAP neurons in leptin signalling. Further, attempts have been made here to characterise this subtype of VMN neuron by using two GFP-reporter lines: Adcyap1-eGFP and PACAP-i-cre X Z/EG transgenic mouse lines. These were used to study the responsiveness of PACAP neurons to fluctuations in glucose availability, and our very promising early results indicate that PACAP VMN neurons are glucose inhibited. We studied the anorectic effects of PACAP and the peptide’s downstream targets, including the corticotrophin-releasing hormone (CRH), melanocortin and oxytocin pathways. The anorexic effect of central PACAP were maintained in VPAC1 and VPAC2 receptor (which also binds the related VIP) knockout animals, implicating the PAC1 receptor as the mediator of the hyperphagic response. We also showed that the feeding effects of PACAP are mediated by CRH, rather than by melanocortin or oxytocin pathways. Finally, we utilised a systems-genetics approach in the BXD set of recombinant inbred mouse strains, in an attempt to tease apart underlying networks of genes contributing to metabolic phenotypes. Quantitative trait analysis identified several loci, which contained genes of potential interest (for example: a QTL related to adiposity contained the orphan G-protein-coupled receptor, GPRC5C). Joint mapping revealed that the phenotypic traits we measured correlated with each other and with trait data from BXD mice recorded in other laboratories. For example, this supported the role of PACAP and BDNF in body-weight management. The candidate gene, gprc5c, was further investigated. Its mRNA was found in the hypothalamus, but was also widely distributed in peripheral tissues. Gprc5c mRNA was regulated by HED in normal C57 mice in the hypothalamus, liver and brown adipose tissue, indicating a possible role for this orphan receptor in metabolism. In fact, similar to PACAP and BDNF, in BXD mice, expression of gprc5c in the hypothalamus was inversely correlated with body-weight gain.
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Caron, Emilie. "Leptine et régulation hypothalamique de la fonction de reproduction chez la souris : sites d'action et influence de la nutrition postnatale." Lille 2, 2006. http://www.theses.fr/2006LIL2S052.

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L'hypothalamus joue un rôle critique dans la régulation des systèmes physiologiques notamment dans le contrôle de la prise alimentaire et de la reproduction. Plus particulièrment il relaie au niveau central le signal leptine, hormone produite et sécrétée par les adipocytes. Alors que les sites d'action de la leptine pour réguler au niveau central la prise alimentaire sont bien caractérisés chez le rat, les sites d'action centraux de la leptine chez la souris au cours du développement postnatal et à l'âge adulte restent mal connus. Nous avons donc analysé la répartition des ARNm de la forme longue du récepteur à la leptine, LepRb, à travers le cerveau de souris au cours du développement postnatal et chez l'adulte. Nous avons ainsi observé que les transcrits de LepRb sont majoritairement exprimés dans l'hypothalamus avec les plus hauts niveaux d'expression détectés dans le noyau arqué. Dans la région préoptique de l'hypothalamus, connue pour réguler la reproduction, l'expression des transcrits de LepRb est restreinte au niveau de l'organe vasculaire de la lame terminale. Les niveaux élevés d'expression des ARNm de LepRb dans le noyau arqué, nous ont amené à émettre l'hypothèse que la plupart des effets centraux de la leptine sur la fonction de reproduction serait véhiculée par ce noyau. Afin de tester cette hypothèse, nous avons évalué la capacité de la leptine à activer les neurones de la région préoptique (via l'induction du proto-oncogène cFos, marqueur d'activité cellulaire) chez des souris sauvages adultes intactes ou chez qui le noyau arqué a été détruit. Par ce biais, nous avons montré que l'activation des neurones de la région préoptique par la leptine nécessite un noyau arqué intact. En accord avec ces résultats, nous avons également mis en évidence que les neurones de la région préoptiques activés par la leptine recevaient une forte innervation en provenance des neurones du noyau arqué. Ces résultats suggèrent un rôle important du noyau arqué dans la transmission des effets centraux de la leptine sur la fonction de reproduction. Ces résultats, associés à des données récentes impliquant le pic néonatal de leptine dans la mise en place des projections du noyau arqué, suggèrent qu'une altération des taux de leptine pendant les premières semaines de vie postnatale pourrait avoir des effets délétères à long terme sur la fonction de reproduction. Afin de tester cette hypothèse, nous avons étudié l'impact de variations de leptinémie induites par une modification des apports nutritionnels pendant le développement postnatal sur la maturation sexuelle. Nous montrons qu'une hypolptinémie induit des perturbations à long terme de la maturation sexuelle et de la fertilité. Ce travail met en évidence pour la première fois les sites anatomiques qui médient au niveau central le signal leptine sur la fonction de reproduction et suggère l'existence d'une " empreinte métabolique ", qui serait véhiculée par la leptine postnatale, sur la fonction de reproduction.
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Sinet, Flore. "Rôle de la néoglucogenèse intestinale dans les comportements émotionnels." Thesis, Lyon, 2016. http://www.theses.fr/2016LYSE1196.

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Le diabète de type 2 et la dépression sont des problèmes majeurs de santé publique associés par un lien bidirectionnel. La dérégulation de l'axe hypothalamo-hypophyso-surrénalien (HPA), accompagnée par un taux élevé de glucocorticoïdes circulants, pourrait constituer un mécanisme commun à ces pathologies. L'axe HPA est régulé principalement au niveau de l'hypothalamus, siège de régulations nutritionnelles et émotionnelles. En ciblant les noyaux hypothalamiques, la néoglucogenèse intestinale (NGI) a des effets bénéfiques contre le développement du diabète de type 2 via la stimulation des nerfs vagal et spinal. Nous avons donc testé si la NGI, par sa communication avec l'hypothalamus, pourrait également réguler les comportements émotionnels et ainsi exercer des effets bénéfiques sur les maladies métaboliques et émotionnelles.L'absence de NGI provoque un dysfonctionnement de l'axe HPA et de son rétrocontrôle négatif (via des modifications moléculaires), caractérisés par une hypersécrétion de glucocorticoïdes et le développement d'une résistance aux glucocorticoïdes. Grâce à des études comportementales et moléculaires, nous montrons que les souris dépourvues de NGI développent des altérations phénotypiques et neurobiologiques caractéristiques d'un état anxio-dépressif. La restauration de la NGI par une perfusion de glucose portale rétablit les altérations neurobiologiques de l'axe HPA. L'induction de la NGI par un régime riche en protéines exerce des effets anxiolytiques et antidépresseurs. Ces données suggèrent que la NGI en ciblant l'hypothalamus, contrôle le métabolisme et, via l'axe HPA, les comportements émotionnels
Type 2 diabetes and major depressive disorder are major health concerns, which are highly comorbid. Hypothalamic-pituitary-adrenal (HPA) axis dysfunction, associated with elevated circulating levels of glucocorticoids, was suggested to be a common mechanism for those pathologies. The hypothalamus, which mainly regulates the HPA axis, is a key integrative center, playing a role in both metabolic and emotional processes. By targeting hypothalamic nuclei, intestinal gluconeogenesis (IGN) exerts beneficial effects against the development of type 2 diabetes through the stimulation of the vagal and spinal nerves. We therefore evaluated whether IGN, via the hypothalamus, may represent a putative common regulator of metabolic and emotional disorders.In the absence of IGN, mice exhibited HPA axis dysregulation along with decreased glucocorticoid-mediated negative feedback (due to molecular modifications), highlighted by hypercortisolism and glucocorticoid resistance. Using behavioral and molecular studies, we demonstrated that mice lacking IGN displayed phenotypic and neurobiological hallmarks of anxiety/depression-like state. Rescuing IGN by portal glucose infusion reversed neurobiological alterations of the HPA axis. Induction of IGN by a protein-enriched diet had anxiolytic and antidepressant effects. Together, these data raise the possibility that IGN by targeting hypothalamus, controls metabolism and, via the HPA axis, emotional behavior
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Johnson, Philip Lee. "The dorsomedial hypothalamus : stress-related physiology and behaviour." Thesis, University of Bristol, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421100.

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Pirc, Alycia Ann. "Modeling Temperature-Sensitive Neural Networks in the Hypothalamus." The Ohio State University, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=osu1306811701.

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Abel, Ty William. "Gonadal steroids, reproductive aging and the primate hypothalamus." Diss., The University of Arizona, 1999. http://hdl.handle.net/10150/284259.

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The gonadal steroid withdrawal of menopause is associated with neuronal hypertrophy and increased tachykinin gene expression in the hypothalamic infundibular nucleus. Previous studies have shown that secretion of hypothalamic b -endorphin is modified by gonadal steroids, and there are consistent age-related changes in b -endorphin neurons in rodents. Therefore, in situ hybridization was used to determine if the expression of POMC mRNA, the precursor for b -endorphin, is altered in the hypothalamus of postmenopausal women. The number of POMC mRNA-containing neurons/section in the infundibular nucleus was reduced by 65% in postmenopausal women. In contrast, there was no significant difference in the number of neurons expressing POMC gene transcripts in the retrochiasmatic region. Our findings support the hypothesis that the activity of hypothalamic POMC neurons is decreased in the infundibular nucleus of postmenopausal women. In a second study, we examined the effects of hormone replacement therapy (HRT) on the hypothalamus of young, ovariectomized cynomolgus monkeys. HRT dramatically suppressed tachykinin gene expression while having no detectable effects on POMC neurons. These results provide strong support for the hypothesis that alterations in tachykinin neurons in postmenopausal women are secondary to estrogen withdrawal. Conversely, postmenopausal changes in POMC gene expression may reflect hypothalamic aging. Finally, we found no evidence that HRT, in doses designed to mimic currently prescribed regimens, produces signs of estrogen toxicity in the primate infundibular nucleus. Degenerative changes, including neuron loss, have been reported in the arcuate nucleus of aging rodents, and hypothalamic aging has been shown to contribute to reproductive decline in these species. In addition, in the infundibular nucleus of postmenopausal women, there is an age-associated decline in proopiomelanocortin gene expression. To evaluate the possibility of neuron loss associated with reproductive aging, unbiased stereological methods were used to compare the total number of infundibular neurons between groups of premenopausal and postmenopausal women. The mean neuronal volume was increased by 40% in postmenopausal women but there was no change in the total number of neurons. These data suggest that the neuronal hypertrophy observed in the postmenopausal human hypothalamus is not a pathological process secondary to degeneration of adjacent infundibular neurons.
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Rochdi, Laïla. "Polymorphisme moleculaire de la gnrh dans l'hypothalamus de rat : consequences sur la secretion hypothalamique et la fonction gonadotrope au cours de l'ontogenese (doctorat : neurosciences)." Aix-Marseille 2, 2000. http://www.theses.fr/2000AIX20654.

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Barbotin, Anne-Laure. "Plasticité neuro-structurale de l’hypothalamus dans le syndrome des ovaires polykystiques." Thesis, Lille, 2019. http://www.theses.fr/2019LILUS043.

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L’hormone anti-Müllerienne (AMH) dont les taux dans le sérum sont élevés dans le Syndrome des Ovaires Polykystiques (SOPK) est connue pour augmenter la sécrétion de LH/GnRH. Comme mis en évidence récemment, cette augmentation de la sécrétion de GnRH pourrait être liée à une hyperactivité des neurones à GnRH en réponse à une action directe de l’AMH mais pourrait également s’exercer indirectement via une augmentation des afférences excitatrices sur les neurones à GnRH. Par ailleurs, les tanycytes, qui enchâssent les terminaisons des neurones à GnRH, expriment le récepteur à l’AMH et sont connus pour moduler la plasticité neuro-structurale de l’hypothalamus. Ainsi, notre objectif est de tester les deux hypothèses suivantes dans un modèle animal et chez la femme. Est-ce que la physiopathologie du SOPK : 1- Est liée à une rétraction des tanycytes provoquée par l’AMH, entraînant l’augmentation des sécrétions de GnRH / LH ? Et/ou 2- Est liée à une augmentation de l’activité des neurones à GnRH AMH-dépendante ?Nous avons étudié la modification de la plasticité morphologique de l’hypothalamus en microscopie électronique en comparant la distance entre les terminaisons des neurones à GnRH et l’espace péri-capillaire entre des éminences médianes de rates en phase de dioestrus de leur cycle oestral (au moment où ces terminaisons sont normalement enfouies par les tanycytes) traitées par de l’AMH et des contrôles. Puis, nous avons comparé cette même distance entre des éminences médianes issues d’un modèle de souris SOPK en comparaison à des contrôles. Enfin, nous avons étudié la plasticité neuro-structurale de l’hypothalamus chez des femmes SOPK et des témoins par une approche en imagerie en comparant les métabolites cérébraux.Nous avons observé une augmentation significative du nombre de terminaisons de neurones à GnRH situées à proximité de l’espace péri-capillaire dans le groupe traité par l’AMH par rapport aux contrôles et nous avons fait les mêmes observations chez les souris SOPK comparées aux contrôles. Par ailleurs, nous avons mis en évidence une augmentation de l’activité neuronale dans le noyau arqué de l’hypothalamus chez des souris SOPK. Or, cette région est particulièrement impliquée dans la régulation de la sécrétion de GnRH. Chez les femmes atteintes de SOPK, nous avons pour la première fois mis en évidence des concentrations plus élevées de GnRH mesurées par spectroscopie de masse par rapport à des femmes normo-ovulantes. Notre étude par IRM, chez les femmes SOPK et contrôles, vient conforter ce résultat en montrant une augmentation de la viabilité/activité neuronale. Cette étude translationnelle suggère que l’augmentation des sécrétions de GnRH/LH rencontrées dans le SOPK serait dépendante d’une part d’un rapprochement de terminaisons à GnRH à l’espace péri-capillaire et d’autre part d’une augmentation de l’activité neuronale hypothalamique
Polycystic ovary syndrome (PCOS) is the most common reproductive disorder (10% of women worldwide). Anti-Müllerian hormone (AMH) levels are found to be 2-3-fold higher in PCOS women than in those with normal ovaries. AMH induces LH secretion by stimulating the activation of GnRH secretion. As recently demonstrated, this increase in GnRH secretion could be related to hyperactivity of GnRH neurons in response to a direct action of AMH but could also be exerted indirectly via an increase in excitatory inputs on GnRH neurons.Our team has previously demonstrated that tanycytes, which unsheathe the terminals of GnRH neurons, regulate GnRH secretion and express AMH receptor. Thus, we aim to determine (1) whether elevated AMH could be responsible for the retraction of the tanycyte coverage leading to increased GnRH/LH secretion in PCOS and (2) whether neuronal hyperactivity in hypothalamus could contribute to higher GnRH activity in PCOS women.Firstly, we have performed ultrastructural studies in rodents’ median eminence (ME) explants challenged with AMH. Then, we compared tanycytic retraction using electron microscopy. We have performed the same experiments in a PCOS mouse model. In humans, we have used metabolic magnetic resonance imaging approaches (i.e. proton magnetic resonance spectra). In order to assess neuronal activity, we have compared N-acetyl-aspartate/creatine ratios in the hypothalamus between PCOS women versus controls.Using electron microscopy, we have shown that tanycytes displayed a significant retraction of their end-feet after AMH treatment ex vivo. This is followed by the sprouting of GnRH terminals towards the pericapillary space. Such processes could significantly favor the sustained delivery of peak levels of GnRH, which could contribute to the rise in LH levels typical of PCOS condition. We have found the same results in PCOS-mouse model with higher GnRH terminals towards the pericapillary space in PCOS mice than in controls. In addition, we found an increase in neuronal activity in the arcuate nucleus of the hypothalamus in PCOS mice. Moreover, this region is particularly involved in the regulation of GnRH secretion. For the first time, we have demonstrated that PCOS women exhibit higher concentrations of GnRH measured by mass spectroscopy than GnRH levels in normo-ovulatory women. Our proton magnetic resonance spectroscopy analysis has revealed that PCOS women exhibit higher N-acetyl aspartate/creatine ratio than controls. These results are predicted to be correlated with increased hypothalamic activity.This translational study suggests that the increase in GnRH / LH secretions found in PCOS could be explained by neurostructural hypothalamic plasticity in link with tanycytes retraction and by an increase of neuronal activity in the hypothalamus
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Books on the topic "Hypothalamus"

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Uwaifo, Gabriel I., ed. The Human Hypothalamus. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62187-2.

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1941-, Ganten D., Pfaff Donald W. 1939-, and Arai Y, eds. Morphology of hypothalamus and its connections. Springer-Verlag, 1986.

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Kenkyūjo, Gunma Daigaku Naibunpi, and Gunma Symposium on Endocrinology (22nd : 1984 : Maebashi-shi, Japan), eds. Hypothalamic peptides in endocrinology: Morphological and physiological aspects. Center for Academic Publications Japan, 1985.

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Trojniar, Weronika. Analiza podłoża morfologicznego wybranych zaburzeń zespołu bocznego podwzgórza u szczura. Uniwersytet Gdański, 1991.

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Altman, Joseph, and Shirley A. Bayer. The Development of the Rat Hypothalamus. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71301-9.

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Ganten, Detlev, and Donald Pfaff, eds. Morphology of Hypothalamus and Its Connections. Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71461-0.

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1940-, Bayer Shirley A., ed. The development of the rat hypothalamus. Springer-Verlag, 1986.

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Derek, Chadwick, and Marsh Joan, eds. Functional anatomy of the neuroendocrine hypothalamus. Wiley, 1992.

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F, Fanardzhi͡a︡n V., ed. Vist͡s︡erosomaticheskie afferentnye sistemy gipotalamusa. Izd-vo "Nauka," Leningradskoe otd-nie, 1985.

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Ağayev, Telman Mämmädäli oğlu. Fiziologiya vä biokimyanin problemläri: Problems of physiology & biochemistry = Problemy fiziologii i biokhimii. Elm, 2008.

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Book chapters on the topic "Hypothalamus"

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Schäffler, A., C. Bollheimer, R. Büttner, et al. "Hypothalamus Hypothalamus." In Funktionsdiagnostik in Endokrinologie, Diabetologie und Stoffwechsel. Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-29690-1_12.

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Schäffler, A., C. Bollheimer, R. Büttner, et al. "Hypothalamus." In Funktionsdiagnostik in Endokrinologie, Diabetologie und Stoffwechsel. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-662-47480-8_12.

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Roberts, P. A. "Hypothalamus." In Oklahoma Notes. Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2902-5_14.

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Waxman, Amanda. "Hypothalamus." In Encyclopedia of Clinical Neuropsychology. Springer New York, 2011. http://dx.doi.org/10.1007/978-0-387-79948-3_1128.

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Beaton, Elliott A. "Hypothalamus." In Encyclopedia of Behavioral Medicine. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1141.

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Orbell, Sheina, Havah Schneider, Sabrina Esbitt, et al. "Hypothalamus." In Encyclopedia of Behavioral Medicine. Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1141.

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McGovern, Amanda. "Hypothalamus." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_1128-2.

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McGovern, Amanda. "Hypothalamus." In Encyclopedia of Clinical Neuropsychology. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_1128.

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Bloch, Michael H., Michael H. Bloch, Mark A. Geyer, et al. "Hypothalamus." In Encyclopedia of Psychopharmacology. Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_1334.

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Roberts, P. A. "Hypothalamus." In Oklahoma Notes. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-0286-5_12.

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Conference papers on the topic "Hypothalamus"

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Trembly, B. Stuart, P. Jack Hoopes, Karen L. Moodie, Gary A. Carson, Marc E. Voorhees, and Jack A. Boulant. "Hypothalamus warming for ischemia protection." In BiOS 2001 The International Symposium on Biomedical Optics, edited by Thomas P. Ryan. SPIE, 2001. http://dx.doi.org/10.1117/12.427861.

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Perov, S. Yu, and S. A. Askerova. "THE NEUROENDOCRINE SYSTEM RESPONSE OF 2-5 G COMMUNICATION ELECTROMAGNETIC FIELD ANIMAL EXPOSURE." In The 16th «OCCUPATION and HEALTH» Russian National Congress with International Participation (OHRNC-2021). FSBSI “IRIOH”, 2021. http://dx.doi.org/10.31089/978-5-6042929-2-1-2021-1-398-402.

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Abstract: Background. The neuroendocrine effect on the hypothalamus-pituitary-adrenal cortex axis is significant example stressor of electromagnetic exposure for biological object. Aim. The neuroendocrine effect investigation of multi-frequency electromagnetic field laboratory animals’ exposure from 2-5 generations cellular base stations Methods. The neuroendocrine status evaluated by corticosterone and adrenocorticotropic hormone (ACTH) concentrations in blood exposed and sham rats. ACTH and corticosterone rat blood assessed by immunoenzyme method. Results. The results of the multi-frequency electromagnetic field laboratory animals’ exposure from 2-5 generations cellular base stations in a chronic experiment showed wave-like changes in the hypothalamic-pituitary-adrenal function. These changes are manifested in an immediate increase in corticosteroids secretion and depression of the corticosteroid response to normal or subnormal levels. After 3 month chronic exposure there was a secondary rise in hormonal secretion.
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Meng, Hongmei, Yudan Lv, Li Cui, et al. "Hypothalamus mediates the cardiovascular changes induced by insular epilepsy." In 2011 International Conference on Human Health and Biomedical Engineering (HHBE). IEEE, 2011. http://dx.doi.org/10.1109/hhbe.2011.6027962.

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Mikhailova, Elena, and Irina Romanova. "SEROTONIN BIOSYNTHESIS SYSTEMS IN THE MICE HYPOTHALAMUS IN OBESITY." In XVII INTERNATIONAL INTERDISCIPLINARY CONGRESS NEUROSCIENCE FOR MEDICINE AND PSYCHOLOGY. LCC MAKS Press, 2021. http://dx.doi.org/10.29003/m2235.sudak.ns2021-17/264-265.

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Vigo, Vera, Maximiliano Nunez, Yuanzhi Xu, Aaron A. Cohen-Gadol, and Juan Carlos Fernandez-Miranda. "Microsurgical Anatomy of the Hypothalamus Applied to Craniopharyngioma Resection." In 31st Annual Meeting North American Skull Base Society. Georg Thieme Verlag KG, 2022. http://dx.doi.org/10.1055/s-0042-1743658.

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Vesnovsky, Oleg, L. D. Timmie Topoleski, Laurence W. Grossman, Jon P. Casamento, and Liang Zhu. "Evaluation of Temperature Transients at Various Body Temperature Measuring Sites Using a Fast Response Thermistor Bead Sensor." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14065.

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Body temperature monitoring of humans has been an important tool for helping clinicians diagnose infections, detect fever, monitor thermoregulation functions during surgical procedures, and assess post-surgery recovery.1–3 Fever itself is typically not considered a disease. It is a response of the body to a disease, which is often inflammatory in nature. Elevation of the set point at the body temperature control center, the brain hypothalamus, is caused by circulating pyrogens produced by the immune system responding to diseases. Since the brain hypothalamus is not easily accessed by thermometers, other body locations have been identified as alternative measuring sites. Those sites include the pulmonary artery, rectum, bladder, distal esophagus and nasopharynx, sublingual surface of the tongue, under the armpit, tympanic membrane, and forehead.
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Pornsawad, Pornsarp. "The feedforward-feedback system of the hypothalamus-pituitary-adrenal axis." In 2013 International Conference on Advances in Computing, Communications and Informatics (ICACCI). IEEE, 2013. http://dx.doi.org/10.1109/icacci.2013.6637379.

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Uluaydin, Niyazi K., Osman Cerezci, and Selim S. Seker. "Can Mobile Phone Usage Affect Hypothalamus-Pituitary-Adrenal Axis Response?" In 2020 10th Annual Computing and Communication Workshop and Conference (CCWC). IEEE, 2020. http://dx.doi.org/10.1109/ccwc47524.2020.9031168.

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Yan, Bin. "Role of Anti-Müllerian Hormone (AMH) in Regulating Hypothalamus-Pituitary Function." In ICBBE '20: 2020 7th International Conference on Biomedical and Bioinformatics Engineering. ACM, 2020. http://dx.doi.org/10.1145/3444884.3444899.

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Popkovsky, N. A., A. D. Lisovsky, D. A. Lisovsky, et al. "Volumetric reconstruction of kisspeptin-producing nuclei of the hypothalamus in rats." In II Международная конференция, посвящеенная 100- летию И.А. Држевецкой. СКФУ, 2022. http://dx.doi.org/10.38006/9612-62-6.2022.252.255.

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Reports on the topic "Hypothalamus"

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Gothilf, Yoav, Yonathan Zohar, Susan Wray, and Hanna Rosenfeld. Inducing sterility in farmed fish by disrupting the development of the GnRH System. United States Department of Agriculture, 2007. http://dx.doi.org/10.32747/2007.7696512.bard.

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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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Ori, Naomi, and Sarah Hake. Similarities and differences in KNOX function. United States Department of Agriculture, 2008. http://dx.doi.org/10.32747/2008.7696516.bard.

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Hypothalamic gonadotropinreleasing hormone (GnRH1) is the key hormone in the control of gametogenesis and gonadal growth in vertebrates. Developmentally, hypothalamic GnRHproducing neurons originate from the olfactory placode, migrate along olfactory axons into the forebrain, and continue to the preoptic area and hypothalamus where they function to stimulate gonadotropin secretion from the pituitary gland. An appropriate location of GnRH neurons within the hypothalamus is necessary for normal reproductive function in the adult; abnormal migration and targeting of GnRH neurons during embryogenesis results in hypogonadism and infertility. The developmental migration of GnRH neurons and axonal pathfinding in mammals are modulated by a plethora of factors, including receptors, secreted molecules, adhesion molecules, etc. Yet the exact mechanism that controls these developmental events is still unknown. We investigated these developmental events and the underlying mechanisms using a transgenic zebrafish model, Tg(gnrh1: EGFP), in which GnRH1 neurons and axons are fluorescently labeled. The role of factors that potentially affect the development of this system was investigated by testing the effect of their knockdown and mutation on the development of the GnRH1 system. In addition, their localization in relation to GnRH1 was described during development. These studies are expected to generate the scientific foundation that will lead to developing innovative technologies, based on the disruption of the early establishment of the GnRH system, for inducing sterility in farmed fish, which is highly desirable for economical and environmental reasons.
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Hristov, Milen, Boycho Landzhov, Kalina Kamenova, and Krassimira Yakimova. Diet-induced Obese Rats Are Associated with Leptin Resistance in the Medial Preoptic Area of the Anterior Hypothalamus. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, 2020. http://dx.doi.org/10.7546/crabs.2020.05.17.

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Meiri, Noam, Michael D. Denbow, and Cynthia J. Denbow. Epigenetic Adaptation: The Regulatory Mechanisms of Hypothalamic Plasticity that Determine Stress-Response Set Point. United States Department of Agriculture, 2013. http://dx.doi.org/10.32747/2013.7593396.bard.

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Our hypothesis was that postnatal stress exposure or sensory input alters brain activity, which induces acetylation and/or methylation on lysine residues of histone 3 and alters methylation levels in the promoter regions of stress-related genes, ultimately resulting in long-lasting changes in the stress-response set point. Therefore, the objectives of the proposal were: 1. To identify the levels of total histone 3 acetylation and different levels of methylation on lysine 9 and/or 14 during both heat and feed stress and challenge. 2. To evaluate the methylation and acetylation levels of histone 3 lysine 9 and/or 14 at the Bdnfpromoter during both heat and feed stress and challenge. 3. To evaluate the levels of the relevant methyltransferases and transmethylases during infliction of stress. 4. To identify the specific localization of the cells which respond to both specific histone modification and the enzyme involved by applying each of the stressors in the hypothalamus. 5. To evaluate the physiological effects of antisense knockdown of Ezh2 on the stress responses. 6. To measure the level of CpG methylation in the promoter region of BDNF in thermal treatments and free-fed, 12-hour fasted, and re-fed chicks during post-natal day 3, which is the critical period for feed-control establishment, and 10 days later to evaluate longterm effects. 7. The phenotypic effect of antisense “knock down” of the transmethylaseDNMT 3a. Background: The growing demand for improvements in poultry production requires an understanding of the mechanisms governing stress responses. Two of the major stressors affecting animal welfare and hence, the poultry industry in both the U.S. and Israel, are feed intake and thermal responses. Recently, it has been shown that the regulation of energy intake and expenditure, including feed intake and thermal regulation, resides in the hypothalamus and develops during a critical post-hatch period. However, little is known about the regulatory steps involved. The hypothesis to be tested in this proposal is that epigenetic changes in the hypothalamus during post-hatch early development determine the stress-response set point for both feed and thermal stressors. The ambitious goals that were set for this proposal were met. It was established that both stressors i.e. feed and thermal stress, can be manipulated during the critical period of development at day 3 to induce resilience to stress later in life. Specifically it was established that unfavorable nutritional conditions during early developmental periods or heat exposure influences subsequent adaptability to those same stressful conditions. Furthermore it was demonstrated that epigenetic marks on the promoter of genes involved in stress memory are altered both during stress, and as a result, later in life. Specifically it was demonstrated that fasting and heat had an effect on methylation and acetylation of histone 3 at various lysine residues in the hypothalamus during exposure to stress on day 3 and during stress challenge on day 10. Furthermore, the enzymes that perform these modifications are altered both during stress conditioning and challenge. Finally, these modifications are both necessary and sufficient, since antisense "knockdown" of these enzymes affects histone modifications, and as a consequence stress resilience. DNA methylation was also demonstrated at the promoters of genes involved in heat stress regulation and long-term resilience. It should be noted that the only goal that we did not meet because of technical reasons was No. 7. In conclusion: The outcome of this research may provide information for the improvement of stress responses in high yield poultry breeds using epigenetic adaptation approaches during critical periods in the course of early development in order to improve animal welfare even under suboptimum environmental conditions.
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Palazzolo, D. L., and K. S. Kumar. Effects of S-2-(3-Methylaminopropylamino)ethyl Phosphorothioic Acid (WR- 3689), Alone or Combined with Caffeine, on Catecholamine Content of Mouse Hypothalamus. Defense Technical Information Center, 1993. http://dx.doi.org/10.21236/ada268505.

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ชินธเนศ, วิไล, บังอร ฉางทรัพย์ та จุฬาลงกรณ์มหาวิทยาลัย คณะแพทยศาสตร์. ภาควิชากายวิภาคศาสตร์. การกระจายของ คาลบินดิน-ดี 28เค และ พารวาลบูมิน ในเซลล์ประสาท โดยวิธีอิมมูโนฮิสโตเคมี ในสมองของกระแต (Tupaia glis) : รายงานการวิจัย. จุฬาลงกรณ์มหาวิทยาลัย, 1995. https://doi.org/10.58837/chula.res.1995.14.

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ได้ทำการศึกษาการกระจายของ calcium binding protein ทั้งสองชิดคือ คาลบินดิน - ดี 28 เค และพารวาลบูมิน ในสมองกระแต (Tupaia glis) โดยวิธี peroxidase-antiperoxidase antidoby ที่ใช้ได้แก่ monoclonal antobody ซึ่งมีความเฉพาะกับ คาลบินดิน - ดี 28 เค และพารวาลบูมิน โดยใช้กระแตไม่จำกัด เพศ น้ำหนัก 130-200 กรัม จำนวน 8 ตัว แบ่งเป็น 4 กลุ่ม กลุ่มละ 2 ตัว ได้แก่กลุ่มซึ่งย้อม คาลบินดินดี 28 เค และตัดตามแนวขวาง กลุ่มซึ่งย้อมคาลบินดิน - ดี 28 เค และตัดตามแนวยาว กลุ่มซึ่งย้อมพารวาลบูมิน และตัดตามแนวขวาง และกลุ่มซึ่งย้อมพารวาลบูมิน และตัดตามแนวยาวจากการทดลองพบว่ามี immunoreactivity ของโปรตีนทั้งสองชนิดนี้ กระจายทั่วไปอย่างกว้างขวางตลอดทั้งสมอง โดยพบในกลุ่มเซลล์ประสาทเกือบทั้งหมด และอยู่ใน perikarya dendrites และ axons ซึ่งโปรตีนสองชนิดนี้ให้ผลบวกในเซลล์ซึ่งต่างชนิดกัน ออกไปและมีเพียงเล็กน้อยเท่านั้นซึ่งพบในเซลล์เดียวกัน ยกตัวอย่าง เช่น ในเซลล์ Purkinje ของสมอง สมองเล็ก และเซลล์ประสาทของ trapezoid nucleus เป็นต้น จากการศึกษานี้พบว่า เซลล์ประสาทซึ่งให้ผลบวกต่อ การย้อมคาลบินดิน - ดี 28 เค เด่นชัดได้แก่ เซลล์ประสาทใน thalamus, hypothalamus, limbic system, sensory system, superior olive, olfactory system, trapezoid nucleus, medial geniculate nucleus, visual system, cerebral cortex, cerebellar cortex และใน extrapyramidal system ส่วนเซลล์ประสาทซึ่งให้ผลบวกต่อการย้อม พารวาลบูมิน ได้แก่ เซลล์ประสาทใน pyramidal system, reticular formation, cerebellar nuclei, cerebellar cortex, cerebral cortex, vestibular system, hippocampal formation และ extrapyramidal system โดยโปรตีนสองชนิดนี้พบได้จำกัดเฉพาะในเซลล์ประสาทและในบางบริเวณของ ependymal cells แต่จะไม่พบในพวก glial cells เลย จากการศึกษาพอจะสรุปได้ว่าโปรตีนทั้งสองชนิดนี้มีการกระจายในกลุ่มเซลล์ประสาท ที่แตกต่างกันเป็นส่วนใหญ่
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ธรรมเจริญ, สัมพันธ์, та ปรมัตถ์ กิจจานุกิจวัฒนา. กลไกการกระตุ้น ERα โดย PPT ต่อพฤติกรรมการกินอาหารและระดับคอติโค โทรปิน รีลิสซิ่งฮอร์โมนในสมองของหนูแรทเพศเมียที่ถูกตัดรังไข่ : รายงานวิจัย. คณะสัตวแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2014. https://doi.org/10.58837/chula.res.2014.71.

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โพรพิลไพราโซลไตรออย (Propyl-pyrazole-triol, PPT) ยับยั้งการกินอาหารอย่างรวดเร็วโดยการกระตุ้นตัวรับฮอร์โมนเอสโตรเจนชนิดแอลฟ่า (estrogen receptor alpha, ERα) ภายในสมอง กลุ่มผู้วิจัยได้เคยรายงานเกี่ยวกับผลการยับยั้งการกินอาหารที่รวดเร็วซึ่งอาจเกี่ยวข้องกับการกระตุ้นเซลล์ประสาทที่สามารถสร้าง คอร์ติโคโทรปิน รีลิ่สซิ่ง ฮอร์โมน (Corticotropin releasing hormone, CRH) ที่สมองส่วนพาราเวนตริคูล่านิวเคลียสของไฮโปทาลามัส (paraventricular nucleus of hypothalamus, PVN) โครงการวิจัยฉบับนี้ดำเนินการเพื่อศึกษาความเชื่อมโยงของ CRH ซึ่งเป็นสารสื่อประสาท (neuromediator) และฤทธิ์ยับยั้งการกินอาหารของ PPT ในการทดลองแรกผู้วิจัยแสดงให้เห็นว่าภายใต้สภาวะการทดลองที่ทำการทดลองนี้ PPT ยับยั้งการกินอาหารในหนูพันธุ์วิสต้าเพศเมียที่ถูกตัดรังไข่ดังเช่นที่เคยถูกรายงานโดยมีระยะเวลาการออกฤทธิ์ราว 3 ชั่วโมง หลังการให้สาร และเนื่องจากผู้วิจัยได้เคยรายงานแล้วว่า PPT สามารถกระตุ้นการแสดงออกของโปรตีน ซี ฟอส (c-Fos) ที่บริเวณสมองหลายนิวเคลียส แต่ผลการทดลอง ดังกล่าวมีความเกี่ยวข้องกับการได้รับอาหาร การทดลองในลำดับต่อมา ผู้วิจัยทำการศึกษาผลของ PPT ต่อการกระตุ้นการแสดงออกของ c-Fos โดยที่ไม่มีการให้อาหาร ผลการทดลองพบว่าจำนวนสัญญาณ c-Fos ที่นับได้จากสมองกลุ่มที่ได้รับ PPT ไม่ต่างจากกลุ่มควบคุมในทุกบริเวณ อย่างไรก็ตามเนื่องจากการให้ PPT ด้วยวิธีการดังกล่าวสามารถลดระดับของ อะดรีโนคอร์ติโคโทรปิน ฮอร์โมน (adrenocorticotropin hormone) ผู้วิจัยจึงให้เห็นผลว่าการกระตุ้น ERα โดย PPT เพียงอย่างเดียวไม่สามารถกระตุ้นการแสดงออกของ c-Fos ในสมองได้ ผู้วิจัยดำเนินการวิจัยในลำดับต่อไปโดยศึกษาระดับของ CRH จากตัวอย่างสมองส่วนนิวเคลียนสต่าง ๆ ที่สนใจทั้งจากสมองส่วนหน้าและส่วนหลังในช่วงเวลาเดียวกับที่ PPT ยับยั้งการกินอาหาร ผลการทดลองแสดงให้เห็นว่า PPT มิได้มีผลกระทบต่อระดับของ CRH ในทุกนิวเคลียสจากสมองส่วนไฮโปทาลามัส แต่ระดับของ CRH ที่สมองส่วนท้ายบริเวณ นิวเคลียส แทรกทัสโซลิทาเรียส (nucleus tractus solitaries, NTS) จากกลุ่มที่ได้รับ PPT สูงกว่ากลุ่มควบคุม ในลำดับสุดท้าย ผู้วิจัยดำเนินการทดลองโดยใช้สารต้านตัวรับ CRH (CRH receptor antagonist, α-Helical CRF (9-41)) ปล่อยเข้าสู่สมองส่วนท้ายโดยวิธีการปล่อยสารผ่านสู่ช่องของสมองลำดับที่ 4 (the 4th cererebroventricular infusion, 4th icv) วัตถุประสงค์ของการทดลองนี้เพื่อประเมินกรณีที่ PPT ทำให้ระดับ CRH ที่สมองส่วนท้ายเพิ่มขึ้นในช่วงเวลาเดียวกับฤทธิ์ที่ทำให้การกินอาหารลดลง เป็นที่น่าเสียใจที่ผลการทดลองพบว่าการให้ α-Helical CRF (9-41) โดยวิธีการ 4th icv อย่างต่อเนื่องเข้าสู่สมองส่วนท้ายไม่สามารถต้านฤทธิ์ของ PPT ที่มีต่อการกินอาหารได้ จากผลการทดลองทั้งหมดผู้วิจัยสรุปว่า PPT สามารถกระตุ้นเซลล์ประสาทส่วน PVN ได้ การกระตุ้นเซลล์ประสาทดังกล่าวนี้อาจทำให้ระดับของ CRH เพิ่มขึ้นที่สมองส่วนท้ายบริเวณ NTS ซึ่งเป็นช่วงเวลาเดียวกับที่ออกฤทธิ์ยับยั้งการกินอาหาร
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8

Dayger Forbes, Catherine. Why Do Animals Do What They Do, When They Do It? Characterizing the Role of the Hypothalamus-Pituitary-Adrenal Axis in Seasonal Life-History Transitions. Portland State University Library, 2000. http://dx.doi.org/10.15760/etd.5506.

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He, zhe, liwei Xing, ming He, yuhuan Sun, jinlong Xu, and rong Zhao. Effect of Acupuncture on Mammary Gland Hyperplasia (MGH): a Bayesian network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.9.0058.

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Review question / Objective: This review aims at conducting a network meta-analysis to assess the potential therapeutic effectiveness and safety of acupuncture therapy for the treatment of MGH. Condition being studied: MGH is a benign breast disease caused by excessive growth of mammary duct epithelial cells and interstitial fibers. Its prevalence rate among women of childbearing age is about 13.5-42%, accounting for 99.3% of the total number of patients with breast related diseases, and its possibility of developing breast cancer can reach 5-10%. Breast hyperplasia can cause clinical symptoms such as breast pain, breast lump, nipple pigmentation and mood fluctuation, which brings severe physical and mental burden to patients. Modern medicine believes that the pathogenesis of MGH is related to sexual hormone disorder secondary to hypothalamus pituitary ovary axis dysfunction.At present, the treatment options of MGH are limited and not completely effective. The commonly used drugs in clinical practice, such as tamoxifen, danazol and goserelin, are expensive, which may lead to breast pain, swelling and increase of interstitial fibrous nodules, and the long-term use of MGH has huge side effects. The clinical guidelines recommend that the use time should be 2 to 6 months. Therefore, it is necessary to seek a treatment method of MGH that is effective, stable and safe.
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Sutcliffe, J. G. Molecular Approach to Hypothalamic Rhythms. Defense Technical Information Center, 1995. http://dx.doi.org/10.21236/ada295080.

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