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Littérature scientifique sur le sujet « Tanyctes »
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Articles de revues sur le sujet "Tanyctes"
Yoo, Sooyeon, Juhyun Kim, Pin Lyu, Thanh V. Hoang, Alex Ma, Vickie Trinh, Weina Dai et al. « Control of neurogenic competence in mammalian hypothalamic tanycytes ». Science Advances 7, no 22 (mai 2021) : eabg3777. http://dx.doi.org/10.1126/sciadv.abg3777.
Texte intégralWittmann, Gabor, Surbhi Gahlot, Malcolm James Low et Ronald M. Lechan. « Rax Expression Identifies a Novel Cell Type in the Adult Mouse Hypothalamus ». Journal of the Endocrine Society 5, Supplement_1 (1 mai 2021) : A42. http://dx.doi.org/10.1210/jendso/bvab048.082.
Texte intégralBolborea, Matei, Marie-Pierre Laran-Chich, Kamontip Rasri, Herbert Hildebrandt, Piyarat Govitrapong, Valérie Simonneaux, Paul Pévet, Stephan Steinlechner et Paul Klosen. « Melatonin Controls Photoperiodic Changes in Tanycyte Vimentin and Neural Cell Adhesion Molecule Expression in the Djungarian Hamster (Phodopus sungorus) ». Endocrinology 152, no 10 (16 août 2011) : 3871–83. http://dx.doi.org/10.1210/en.2011-1039.
Texte intégralde Vries, E. M., J. Kwakkel, L. Eggels, A. Kalsbeek, P. Barrett, E. Fliers et A. Boelen. « NFκB Signaling Is Essential for the Lipopolysaccharide-Induced Increase of Type 2 Deiodinase in Tanycytes ». Endocrinology 155, no 5 (1 mai 2014) : 2000–2008. http://dx.doi.org/10.1210/en.2013-2018.
Texte intégralJawad, Haider, Muthanna Al-Kaabi et Anam Al-Salihi. « IMMUNOHISTOCHEMICAL EXPRESSION OF MONOCARBOXYLATE TRANSPORTER 1&4 IN TANYCYTE–LIKE CELLS OF THE SULCUS MEDIANUS ORGANUM ». Iraqi Journal of Medical Sciences 17, no 1 (31 mars 2019) : 83–99. http://dx.doi.org/10.22578/ijms.17.1.12.
Texte intégralde Seranno, Sandrine, Xavier d'Anglemont de Tassigny, Cecilia Estrella, Anne Loyens, Sergey Kasparov, Danièle Leroy, Sergio R. Ojeda, Jean-Claude Beauvillain et Vincent Prevot. « Role of Estradiol in the Dynamic Control of Tanycyte Plasticity Mediated by Vascular Endothelial Cells in the Median Eminence ». Endocrinology 151, no 4 (4 février 2010) : 1760–72. http://dx.doi.org/10.1210/en.2009-0870.
Texte intégralBolborea, Matei, Gisela Helfer, Francis J. P. Ebling et Perry Barrett. « Dual signal transduction pathways activated by TSH receptors in rat primary tanycyte cultures ». Journal of Molecular Endocrinology 54, no 3 (30 mars 2015) : 241–50. http://dx.doi.org/10.1530/jme-14-0298.
Texte intégralSánchez, Edith, Praful S. Singru, Gábor Wittmann, Shira S. Nouriel, Perry Barrett, Csaba Fekete et Ronald M. Lechan. « Contribution of TNF-α and Nuclear Factor-κB Signaling to Type 2 Iodothyronine Deiodinase Activation in the Mediobasal Hypothalamus after Lipopolysaccharide Administration ». Endocrinology 151, no 8 (25 mai 2010) : 3827–35. http://dx.doi.org/10.1210/en.2010-0279.
Texte intégralPorniece Kumar, Marta, Anna Lena Cremer, Paul Klemm, Lukas Steuernagel, Sivaraj Sundaram, Alexander Jais, A. Christine Hausen et al. « Insulin signalling in tanycytes gates hypothalamic insulin uptake and regulation of AgRP neuron activity ». Nature Metabolism 3, no 12 (décembre 2021) : 1662–79. http://dx.doi.org/10.1038/s42255-021-00499-0.
Texte intégralBarrett, Perry, Elena Ivanova, E. Scott Graham, Alexander W. Ross, Dana Wilson, Helene Plé, Julian G. Mercer et al. « Photoperiodic regulation of cellular retinoic acid-binding protein 1, GPR50 and nestin in tanycytes of the third ventricle ependymal layer of the Siberian hamster ». Journal of Endocrinology 191, no 3 (décembre 2006) : 687–98. http://dx.doi.org/10.1677/joe.1.06929.
Texte intégralThèses sur le sujet "Tanyctes"
Bellamy, Charlotte. « Functional characterization of a novel mutation in PRKCA, the major driver of Chordoid glioma ». Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASL052.
Texte intégralChordoid glioma (ChG) is a rare low-grade brain tumor, characterised by a novel recurrent point mutation PRKCA p.D463H, a substitution in the kinase domain of Protein kinase C alpha (PKCα). This study demonstrates the role of this mutated kinase in the development of ChGs. Here we show the inactivation and dominant negative effect of PKCαD463H via in vitro and In cellulo activity assays. Our results show the mutation affects the tertiary structure, resulting in an open, unstable protein. Phosphoproteomic and Co-Immunoprecipitation mass spectrometry data from HEK cells overexpressing PKC⍺D463H show decreased phosphorylation and interaction with proteins involved in cell adhesion. We confirm genetically through single nuclei RNAseq that ChGs derive from specialised tanycytes. By understanding the cell context of tumorigenesis alongside the functional changes of this mutation on the activity and interactome of PKCα, we elaborated a model of the development of ChGs alongside the identification of a therapeutic approach
Benford, Heather Elizabeth. « Signalling in hypothalamic tanycytes ». Thesis, University of Warwick, 2014. http://wrap.warwick.ac.uk/62112/.
Texte intégralLazutkaite, Greta. « Amino acid sensing in hypothalamic tanycytes via umami taste receptors ». Thesis, University of Warwick, 2018. http://wrap.warwick.ac.uk/109627/.
Texte intégralCappellini, Prieto Monica. « Transplantation de tanycytes dans la moelle épinière de rats adultes ». Montpellier 2, 2000. http://www.theses.fr/2000MON20109.
Texte intégralBalland, Églantine. « Rôle des tanycytes de l’éminence médiane dans le transport de la leptine de la périphérie vers l’hypothalamus ». Thesis, Lille 2, 2012. http://www.theses.fr/2012LIL2S053.
Texte intégralThe arcuate nucleus of the hypothalamus (ARH) is a critical component of the neural circuits that regulate energy balance. However, little is known about how peripheral signals reach the ARH to mediate their central effects. The ARH is adjacent to the median eminence (ME), where highly specialized ependymal cells called tanycytes are found. The cell bodies of tanycytes are lining the floor of the third ventricle and their end-feet are contacting the rich capillary plexus with fenestrated endothelium of the ME. Tanycytes have recently been proposed to play a role in blood-hypothalamus barrier regulation. Their privileged location at the interface between the blood and the brain suggests that these cells might be direct target for a variety of peripheral signals, including the adipocyte-derived hormone leptin. The understanding of leptin transport mechanisms is fundamental as it may provide new insights into cellular processes involved in leptin resistance linked to obesity.The aim of this work was to determine wether tanycytes of the median eminence could be responsible for leptin entry in the hypothalamus and in this case if they could be involved in the mechanisms responsible for obesity-associated leptin resistance.We first investigated leptin uptake into the hypothalamus through several approaches in vivo. Western-blot experiments revealed that peripherally injected leptin is sequentially found in ME and later in MBH, moreover the timing of the leptin receptor activation appears to follow the same sequence. In contrast, we observed that leptin failed to reach the hypothalamus and was seen to accumulate in the ME in obese mice (db/db and DIO models) that has lost the capacity of activating LepRb signaling pathways in the ME. The use of fluorescent leptin demonstrated that leptin is internalized in ΜΕ tanycytes in a polarized manner, leptin is uptaken at the level of the basal processes contacting fenestrated capillaries and transported toward the apical pole. In addition, we showed that these tanycytes are the first cell type in the median eminence to respond to peripheral leptin injection through the activation of P-STAT3 detected by immunohistochemistry. The use of a leptin antagonist showed the dependence of leptin receptor(s) activation for leptin internalization in tanycytes. Then, the use of tanycyte primary cultures as an in vitro model system allowed us to study leptin transport mechanisms more in detail. Experiments performed on cultured tanycytes confirmed our in vivo findings and showed that the release of leptin from tanycytes, which is blocked in obese mice, depends on the activation of the X signaling pathway. The use of a pharmacological compound able to activate the X signaling pathway in tanycytes can rescue leptin transport from ME to MBH in obese mice. Altogether this data may provide valuable information in the understanding of central leptin transport and may help to explain mechanism underlying obesity-associated leptin resistance
Barbotin, Anne-Laure. « Plasticité neuro-structurale de l’hypothalamus dans le syndrome des ovaires polykystiques ». Thesis, Lille, 2019. http://www.theses.fr/2019LILUS043.
Texte intégralPolycystic 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
Mullier, Amandine. « Etude des interfaces sang/cerveau dans la région tubérale de l'hypothalamus médiobasal : rôle des tanycytes de l'éminence médiane ». Phd thesis, Université du Droit et de la Santé - Lille II, 2009. http://tel.archives-ouvertes.fr/tel-00515862.
Texte intégralChauvet, Norbert. « Rôles des tanycytes dans les mécanismes de régénération axonale des neurones du système nerveux central du rat adulte ». Montpellier 2, 1997. http://www.theses.fr/1997MON20160.
Texte intégralChaker, Zayna. « Longevity gene IGF-1 and adult neurogenesis : regulation of lifelong neuronal replacement, olfactory function and metabolism ». Thesis, Paris 5, 2014. http://www.theses.fr/2014PA05T052.
Texte intégralProduction of new neurons in the brain decreases dramatically with age due to progressive physiological depletion of stem and progenitor cell populations (NSCs). Recent studies indicate that circulating factors constitute a systemic aging milieu regulating the birth of new cells. Interestingly, some long-lived mouse strains such as Ames dwarf mutants, with low circulating levels of GH and IGF-1, show increased neurogenesis and preserved hematopoietic stem cell pool. Thus, the possibility that genes regulating lifespan and aging also quantitatively modulate stem cells in mammals is more and more explored. IGF-1 plays a pivotal role in aging in different species, and I am asking whether some of the well-known longevity effects resulting from down-regulation of this signaling pathway could be explained by local regulation of stem and progenitor cell compartments. To validate this hypothesis, I pursued a dual approach based on biological experiments and mathematical modeling. Using a novel triple transgenic mouse model, I inactivated IGF-1 signaling specifically in adult NSCs, and traced knockout cell lineages with a fluorescent reporter transgene. By analyzing the phenotype at different time points after KO induction, I could distinguish between short and long-term effects of IGF signaling on cellular regeneration and identify cumulative physiological consequences of down-regulation of this pathway using behavioral tests. In my mathematical models, the dynamics of regenerative cell populations were described by a set of differential equations depending on circulating “growth-factor like molecules” (GFs). My results suggest that in aging tissues, the optimal distribution of GFs is a function that decreases with time. In the olfactory system, I showed that inactivation of IGF signaling in adult NSCs enhanced long-term maintenance of neuroblasts and increased the overall production of neurons. Mutants started with the same number of adult-born neurons as controls one month after KO induction at 4 months of age, but ended up having significantly more differentiated cells integrating the olfactory bulb at long-term, i.e. at 16 months of age. This highly increased neurogenic activity occurred without depletion of neural stem/progenitor cell compartments. In contrast, IGF-1R deletion in adult hippocampal stem cells did not change neurogenesis dynamics, pointing out a niche-dependent effect of IGFs. The important cellular changes in the olfactory bulb led to improved olfactory memory and odor discrimination in aged mutants. Strikingly, mutants also displayed altered energy homeostasis and increased sensitivity to metabolic hormones, namely leptin and insulin. This metabolic shift could be linked to enhanced olfactory function, and to changes in hypothalamic neurogenesis. Indeed, we observed that IGF-1R deletion in hypothalamic stem cells (HySC) protected α-tanycyte pool from age-related decline and increased the number of newborn neurons in the hypothalamus. Taken together, my results validate the hypothesis that life-long inhibition of IGF signaling in adult NSCs delays age-related decline of neurogenesis, in a niche-dependent manner. These data also show that local modulation of neural cell replacement has important physiological effects at the level of the whole organism, pointing out a novel pathophysiological role for adult neurogenesis
Milesi, Sébastien. « Rôle de la signalisation hypothalamique TSH/T3 dans la reproduction saisonnière chez les hamsters Djungariens (Phodopus sungorus) et Syriens (Mesocricetus auratus) ». Thesis, Strasbourg, 2018. http://www.theses.fr/2018STRAJ023/document.
Texte intégralIn hamsters, reproduction is activated by long days. This photoactivation (PA) supposedly involves melatonin, hypothalamic thyroid hormones (TH) and RFamide peptides. Maintaining inhibitory short days for over 20 weeks triggers a photorefractory reactivation of the hypothalamo pituito gonadotropic axis (HPG) The mechanisms of this PR are so far unknown. Our cinetic analysis of the dynamic molecular changes in PA and PR revealed a conserved early inhibition of tanycytic deiodinase 3 (Dio3), which catabolizes TH, in both activation mechanisms. Associated with a late decrease of the TH transporter MCT8, the inhibition of Dio3 could generate an early peak of hypothalamic TH. In both activations, RFamide upregulation occurs several weeks after the initial Dio3 inhibition. Also, pharmacological inhibition of RFRP3 during PA does not influence the HPG activity, questioning the role of RFRP3 in HPG activation. We have thus uncovered a so far unreported early Dio3 inhibition that could be sufficient to seasonally reactivate the gonadotropic axis. The seasonal regulator of Dio3 remains to be discovered
Chapitres de livres sur le sujet "Tanyctes"
Lechan, Ronald M., et Csaba Fekete. « Tanycyte Regulation of Hypophysiotropic TRH Neurons ». Dans Masterclass in Neuroendocrinology, 285–307. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62383-8_12.
Texte intégralBarrett, Perry, et Peter J. Morgan. « Tanycytes and Their Pivotal Role in Seasonal Physiological Adaptations ». Dans Neuroendocrine Clocks and Calendars, 55–84. Cham : Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-55643-3_3.
Texte intégralNampoothiri, Sreekala, Manon Duquenne et Vincent Prevot. « Unveiling the Importance of Tanycytes in the Control of the Dialogue Between the Brain and the Periphery ». Dans Masterclass in Neuroendocrinology, 255–84. Cham : Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-62383-8_11.
Texte intégralBlackshaw, Seth, Daniel A. Lee, Thomas Pak et Sooyeon Yoo. « Regulation of Body Weight and Metabolism by Tanycyte-Derived Neurogenesis in Young Adult Mice ». Dans Stem Cells in Neuroendocrinology, 51–67. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-41603-8_5.
Texte intégralHökfelt, T., G. Foster, M. Schultzberg, B. Meister, M. Schalling, M. Goldstein, H. C. Hemmings, C. Ouimet et P. Greengard. « DARPP-32 as a Marker for D-1 Dopaminoceptive Cells in the Rat Brain : Prenatal Development and Presence in Glial Elements (Tanycytes) in the Basal Hypothalamus ». Dans Advances in Experimental Medicine and Biology, 65–82. Boston, MA : Springer US, 1988. http://dx.doi.org/10.1007/978-1-4899-2723-1_6.
Texte intégralFlament-Durand, J., et J. P. Brion. « Tanycytes : Morphology and Functions : A Review ». Dans International Review of Cytology, 121–55. Elsevier, 1985. http://dx.doi.org/10.1016/s0074-7696(08)60596-3.
Texte intégralBernal, Juan. « Deiodinases in the Brain ». Dans Thyroid and Brain : Understanding the Actions of Thyroid Hormones in Brain Development and Function, 39–64. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815274226124010007.
Texte intégralRAFOLS, JOSÉ A. « EPENDYMAL TANYCYTES OF THE VENTRICULAR SYSTEM IN VERTEBRATES ». Dans Astrocytes, 131–48. Elsevier, 1986. http://dx.doi.org/10.1016/b978-0-12-250451-8.50009-6.
Texte intégralIyer, Lakshmanan K., Joshua A. Ainsley, Csaba Fekete et Ronald M. Lechan. « Digital Expression Profiling of Tanycytes Suggests Molecular Mechanisms for Their Biological Function ». Dans BASIC/TRANSLATIONAL - Pituitary Biology & ; Tumorigenesis, P1–396—P1–396. The Endocrine Society, 2011. http://dx.doi.org/10.1210/endo-meetings.2011.part2.p2.p1-396.
Texte intégralPrevot, Vincent, Ruben Nogueiras et Markus Schwaninger. « Tanycytes in the infundibular nucleus and median eminence and their role in the blood–brain barrier ». Dans The Human Hypothalamus - Middle and Posterior Region, 253–73. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-820107-7.00016-1.
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