Journal articles: 'Tanyctes'

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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 (May 2021): eabg3777. http://dx.doi.org/10.1126/sciadv.abg3777.

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Hypothalamic tanycytes, radial glial cells that share many features with neuronal progenitors, can generate small numbers of neurons in the postnatal hypothalamus, but the identity of these neurons and the molecular mechanisms that control tanycyte-derived neurogenesis are unknown. In this study, we show that tanycyte-specific disruption of the NFI family of transcription factors (Nfia/b/x) robustly stimulates tanycyte proliferation and tanycyte-derived neurogenesis. Single-cell RNA sequencing (scRNA-seq) and single-cell assay for transposase-accessible chromatin sequencing (scATAC-seq) analysis reveals that NFI (nuclear factor I) factors repress Sonic hedgehog (Shh) and Wnt signaling in tanycytes and modulation of these pathways blocks proliferation and tanycyte-derived neurogenesis in Nfia/b/x-deficient mice. Nfia/b/x-deficient tanycytes give rise to multiple mediobasal hypothalamic neuronal subtypes that can mature, fire action potentials, receive synaptic inputs, and selectively respond to changes in internal states. These findings identify molecular mechanisms that control tanycyte-derived neurogenesis, which can potentially be targeted to selectively remodel the hypothalamic neural circuitry that controls homeostatic physiological processes.

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Wittmann, Gabor, Surbhi Gahlot, Malcolm James Low, and Ronald M. Lechan. "Rax Expression Identifies a Novel Cell Type in the Adult Mouse Hypothalamus." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A42. http://dx.doi.org/10.1210/jendso/bvab048.082.

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Abstract Hypothalamic tanycytes are radial glia-like ependymal cells lining the ventrolateral walls and floor of the third ventricle. Recent data show that tanycytes are adult neural stem/progenitor cells, capable of generating neurons that populate the adjacent hypothalamic nuclei involved in the regulation of feeding and energy balance. Thus, the genetic fate mapping of tanycytes has become an invaluable tool to identify and study tanycyte-derived adult-born hypothalamic neurons. Perhaps the most selective tanycyte marker identified to date is the retina and anterior neural fold homeobox (Rax), that has been used as a tanycyte marker in multiple single-cell transcriptomic studies. By using in situ hybridization and immunofluorescence, we show that Rax mRNA and RAX protein are also expressed in a minor but significant population of parenchymal cells that are concentrated in the caudal arcuate nucleus. RAX-positive nuclei in the parenchyma were often observed in pairs, suggesting recent cell divisions. The morphology of these cells was studied in tamoxifen-treated Rax-CreERT2; Ai34(RCL-Syp/tdT)-D mice, in which the synaptophysin-tdTomato fusion protein permanently labels Rax-expressing cells and their progeny. While some parenchymal RAX-positive cells had tanycyte-like morphology indicative of tanycyte migration into the parenchyma, the majority had a very different morphology with extensive local processes that often encircled adjacent neurons (termed “frizzy cells”). The tdTomato labeling also revealed numerous frizzy cells that were negative for RAX, indicating downregulation of endogenous Rax expression subsequent to the induction of synaptophysin-tdTomato reporter expression. Many of these cells were distributed outside the caudal arcuate nucleus, including the rostral lateral arcuate nucleus, ventromedial and dorsomedial hypothalamic nuclei and lateral hypothalamus. RAX-negative frizzy cells were also conspicuous in the paraventricular nucleus, and occasionally observed in the preoptic region and bed nucleus of the stria terminalis. Frizzy cells were negative for the tanycyte-enriched proteins vimentin, monocarboxylate transporter 8 (MCT8) or glial fibrillary acidic protein (GFAP). These results identify a novel Rax-expressing cell type in the adult hypothalamus that differs from tanycytes in location, morphology and gene expression characteristics. Future studies are required to determine whether frizzy cells are derived from tanycytes or constitute a separate cell lineage, and whether they represent a migratory form of neural precursor cells in the adult hypothalamus.

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Bolborea, Matei, Marie-Pierre Laran-Chich, Kamontip Rasri, Herbert Hildebrandt, Piyarat Govitrapong, Valérie Simonneaux, Paul Pévet, Stephan Steinlechner, and 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 (August 16, 2011): 3871–83. http://dx.doi.org/10.1210/en.2011-1039.

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The Djungarian hamster displays photoperiodic variations in gonadal size synchronized to the seasons by the nightly secretion of the pineal hormone melatonin. In short photoperiod (SP), the gonads regress in size, and circulating sex steroids levels decline. Thus, the brain is subject to seasonal variations of both melatonin and sex steroids. Tanycytes are specialized glial cells located in the ependymal lining of the third ventricle. They send processes either to the meninges or to blood vessels of the medio-basal hypothalamus. Furthermore, they are known to locally modulate GnRH release in the median eminence and to display seasonal structural changes. Seasonal changes in tanycyte morphology might be mediated either through melatonin or sex steroids. Therefore, we analyzed the effects of photoperiod, melatonin, and sex steroids 1) on tanycyte vimentin expression by immunohistochemistry and 2) on the expression of the neural cell adhesion molecule (NCAM) and polysialic acid as markers of brain plasticity. Vimentin immunostaining was reduced in tanycyte cell bodies and processes in SP. Similarly, tanycytes and their processes contained lower amounts of NCAM in SP. These changes induced by SP exposure could not be restored to long photoperiod (LP) levels by testosterone supplementation. Likewise, castration in LP did not affect tanycyte vimentin or NCAM expression. By contrast, late afternoon melatonin injections mimicking a SP-like melatonin peak in LP hamsters reduced vimentin and NCAM expression. Thus, the seasonal changes in vimentin and NCAM expression in tanycytes are regulated by melatonin independently of seasonal sex steroid changes.

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de Vries, E. M., J. Kwakkel, L. Eggels, A. Kalsbeek, P. Barrett, E. Fliers, and A. Boelen. "NFκB Signaling Is Essential for the Lipopolysaccharide-Induced Increase of Type 2 Deiodinase in Tanycytes." Endocrinology 155, no. 5 (May 1, 2014): 2000–2008. http://dx.doi.org/10.1210/en.2013-2018.

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The enzyme type 2 deiodinase (D2) is a major determinant of T3 production in the central nervous system. It is highly expressed in tanycytes, a specialized cell type lining the wall of the third ventricle. During acute inflammation, the expression of D2 in tanycytes is up-regulated by a mechanism that is poorly understood at present, but we hypothesized that cJun N-terminal kinase 1 (JNK1) and v-rel avian reticuloendotheliosis viral oncogene homolog A (RelA) (the 65 kD subunit of NFκB) inflammatory signal transduction pathways are involved. In a mouse model for acute inflammation, we studied the effects of lipopolysaccharide (LPS) on mRNA expression of D2, JNK1, and RelA in the periventricular area (PE) and the arcuate nucleus-median eminence of the hypothalamus. We next investigated LPS-induced D2 expression in primary tanycyte cell cultures. In the PE, the expression of D2 was increased by LPS. In the arcuate nucleus, but not in the PE, we found increased RelA mRNA expression. Likewise, LPS increased D2 and RelA mRNA expression in primary tanycyte cell cultures, whereas JNK1 mRNA expression did not change. Phosphorylation of RelA and JNK1 was increased in tanycyte cell cultures 15–60 minutes after LPS stimulation, confirming activation of these pathways. Finally, inhibition of RelA with the chemical inhibitors sulfasalazine and 4-Methyl-N1-(3-phenylpropyl)benzene-1,2-diamine (JSH-23) in tanycyte cell cultures prevented the LPS-induced D2 increase. We conclude that NFκB signaling is essential for the up-regulation of D2 in tanycytes during inflammation.

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Jawad, Haider, Muthanna Al-Kaabi, and 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 (March 31, 2019): 83–99. http://dx.doi.org/10.22578/ijms.17.1.12.

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Background: Circumventricular organs (CVOs) are specialized structures border the brain ventricles and lack the blood-brain barrier. These CVOs are lined by specialized ependymal cells (ECs) called tanycyte. The sulcus medianus organum (SMO) locates at the floor of the 4th ventricle at the rostral part of the sulcus medianus (SM). Objective: To explore the expression of the monocarboxylate transporter 1 and monocarboxylate transporter 4 (MCT1 & MCT4) in the tanycytes of the median eminence (ME) and tanycyte-like cells of the SMO to add a functional evidence for describing the SMO as another CVOs and to start a roadmap for the citing the SMO specifically as a sensory or a secretory CVO. Methods: Ten adult male rats (Rattus norvegicus albinus), aged 3-6 months with 300±50 g, were used to study the histological characteristics of ECs in ME and SMO with Hematoxylin & Eosin and to explore the immunohistochemical expression of MCT1 & MCT4 in ME and SMO. Results: The ependymal cells were arranged in in 2-3 layers in the depth of SMO region and single layer in the ME region as seen with H&E stains. Immunohistochemical expression of MCT1 & MCT4 using Aperioscope image analysis in tanycytes of the ME is higher than that in tanycyte-like cells of the SMO with significant differences between the two regions as proved by t-test. Conclusion: the SMO has different structural and functional properties compared to ME suggesting that the SMO may be a sensory CVO. Keywords: Circumventricular organs, tanycytes, sulcus medianus organum, median eminence Citation: Jawad HF, Al-Kaabi MA, Al-Salihi AR. Immunohistochemical expression of monocarboxylate transporter 1&4 in tanycyte–like cells of the sulcus medianus organum. Iraqi JMS. 2019; 17(1): 83-99. doi: 10.22578/IJMS.17.1.12

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de Seranno, Sandrine, Xavier d'Anglemont de Tassigny, Cecilia Estrella, Anne Loyens, Sergey Kasparov, Danièle Leroy, Sergio R. Ojeda, Jean-Claude Beauvillain, and 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 (February 4, 2010): 1760–72. http://dx.doi.org/10.1210/en.2009-0870.

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In the ever-changing physiological context of the neuroendocrine brain, the mechanisms by which cellular events involving neurons, astroglia, and vascular cells are coordinated to bring forth the appropriate neuronal signaling is not yet known but is amenable to examination. In the median eminence of the hypothalamus, endothelial cells are key players in the plasticity of tanycytes (specialized astroglia) and neuroendocrine synapse efficacy. Here we report that estradiol acts on both purified endothelial cells and isolated tanycytes to trigger endothelial-to-glial communication that leads to a sudden and massive retraction of tanycyte processes. The blockade of endothelial nitric oxide synthase by in vitro adenoviral-mediated gene transfer of a dominant-negative form of endothelial nitric oxide synthase abrogates the estradiol-induced tanycyte plasticity mediated by endothelial cells. In parallel, increases in prostaglandin-E2 (PGE2) due to changes in cyclooxygenase (COX)-1 and COX-2 expression induced by the exposure of tanycytes to estradiol promote acute tanycyte plasticity. We also demonstrate by electron microscopy that the administration of PGE2 to median eminence explants induces rapid neuroglial plasticity at the neurovascular junction of neurons that release GnRH (the neuropeptide controlling reproduction). Conversely, preventing local PGE2 synthesis in the median eminence of adult female rats with the COX inhibitor indomethacin impairs the ovarian cycle, a process that requires a pulsatile, coordinated delivery of GnRH into the hypothalamo-hypophyseal portal system. Taken together, our findings show that estradiol controls the dialog between endothelial cells and astroglia to regulate neuroglial plasticity in the neuroendocrine brain.

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Bolborea, Matei, Gisela Helfer, Francis J. P. Ebling, and Perry Barrett. "Dual signal transduction pathways activated by TSH receptors in rat primary tanycyte cultures." Journal of Molecular Endocrinology 54, no. 3 (March 30, 2015): 241–50. http://dx.doi.org/10.1530/jme-14-0298.

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Tanycytes play multiple roles in hypothalamic functions, including sensing peripheral nutrients and metabolic hormones, regulating neurosecretion and mediating seasonal cycles of reproduction and metabolic physiology. This last function reflects the expression of TSH receptors in tanycytes, which detect photoperiod-regulated changes in TSH secretion from the neighbouringpars tuberalis. The present overall aim was to determine the signal transduction pathway by which TSH signals in tanycytes. Expression of the TSH receptor in tanycytes of 10-day-old Sprague Dawley rats was observed byin situhybridisation. Primary ependymal cell cultures prepared from 10-day-old rats were found by immunohistochemistry to express vimentin but not GFAP and by PCR to express mRNA forDio2,Gpr50,Darpp-32andTshreceptors that are characteristic of tanycytes. Treatment of primary tanycyte/ependymal cultures with TSH (100 IU/l) increased cAMP as assessed by ELISA and induced a cAMP-independent increase in the phosphorylation of ERK1/2 as assessed by western blot analysis. Furthermore, TSH (100 IU/l) stimulated a 2.17-fold increase inDio2mRNA expression. We conclude that TSH signal transduction in cultured tanycytes signals via Gαsto increase cAMP and via an alternative G protein to increase phosphorylation of ERK1/2.

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Sánchez, Edith, Praful S. Singru, Gábor Wittmann, Shira S. Nouriel, Perry Barrett, Csaba Fekete, and 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 (May 25, 2010): 3827–35. http://dx.doi.org/10.1210/en.2010-0279.

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To determine whether signaling through TNF and/or nuclear factor-κB contributes to bacterial lipopolysaccharide (LPS)-induced activation of type 2 iodothyronine deiodinase (D2) in tanycytes lining the floor and infralateral walls of the third ventricle, the effect of a TNF antagonist on D2 gene expression and LPS-induced Iκ-Bα expression in tanycytes were studied. Animals treated with soluble, rat, polyethylene glycol-conjugated TNF receptor type 1 (4 mg/kg body weight) before a single ip injection of LPS showed a significant reduction in circulating IL-6 levels but no effect on LPS-induced D2 mRNA in the majority of tanycytes with the exception of a subpopulation of α tanycytes in the wall of the third ventricle. LPS induced a rapid increase in Iκ-Bα mRNA in the pars tuberalis and a delayed response in α tanycytes but absent in all other tanycyte subsets. The LPS-induced increase in Iκ-Bα in the pars tuberalis was associated with increased TSHβ gene expression in this tissue, but cAMP response element-binding protein (CREB) phosphorylation was observed only in a subset of α tanycytes. These data suggest that TNF and nuclear factor-κB signaling are not the primary, initiating mechanisms mediating the LPS-induced D2 response in tanycytes, but may contribute in part to sustaining the LPS-induced D2 response in a subset of α tanycytes. We hypothesize that in addition to TSH, other factors derived from the pars tuberalis may contribute to LPS-induced D2 activation in tanycytes.

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Porniece 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 (December 2021): 1662–79. http://dx.doi.org/10.1038/s42255-021-00499-0.

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AbstractInsulin acts on neurons and glial cells to regulate systemic glucose metabolism and feeding. However, the mechanisms of insulin access in discrete brain regions are incompletely defined. Here we show that insulin receptors in tanycytes, but not in brain endothelial cells, are required to regulate insulin access to the hypothalamic arcuate nucleus. Mice lacking insulin receptors in tanycytes (IR∆Tan mice) exhibit systemic insulin resistance, while displaying normal food intake and energy expenditure. Tanycytic insulin receptors are also necessary for the orexigenic effects of ghrelin, but not for the anorexic effects of leptin. IR∆Tan mice exhibit increased agouti-related peptide (AgRP) neuronal activity, while displaying blunted AgRP neuronal adaptations to feeding-related stimuli. Lastly, a highly palatable food decreases tanycytic and arcuate nucleus insulin signalling to levels comparable to those seen in IR∆Tan mice. These changes are rooted in modifications of cellular stress responses and of mitochondrial protein quality control in tanycytes. Conclusively, we reveal a critical role of tanycyte insulin receptors in gating feeding-state-dependent regulation of AgRP neurons and systemic insulin sensitivity, and show that insulin resistance in tanycytes contributes to the pleiotropic manifestations of obesity-associated insulin resistance.

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Barrett, 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 (December 2006): 687–98. http://dx.doi.org/10.1677/joe.1.06929.

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Tanycytes in the ependymal layer of the third ventricle act both as a barrier and a communication gateway between the cerebrospinal fluid, brain and portal blood supply to the pituitary gland. However, the range, importance and mechanisms involved in the function of tanycytes remain to be explored. In this study, we have utilized a photoperiodic animal to examine the expression of three unrelated gene sequences in relation to photoperiod-induced changes in seasonal physiology and behaviour. We demonstrate that cellular retinoic acid-binding protein 1 (CRBP1), a retinoic acid transport protein, GPR50, an orphan G-protein-coupled receptor and nestin, an intermediate filament protein, are down-regulated in short-day photoperiods. The distribution of the three sequences is very similar, with expression located in cells with tanycyte morphology in the region of the ependymal layer where tanycytes are located. Furthermore, CRBP1 expression in the ependymal layer is shown to be independent of a circadian clock and altered testosterone levels associated with testicular regression in short photo-period. Pinealectomy of Siberian hamsters demonstrates CRBP1 expression is likely to be dependent on melatonin output from the pineal gland. This provides evidence that tanycytes are seasonally responsive cells and are likely to be an important part of the mechanism to facilitate seasonal physiology and behaviour in the Siberian hamster.

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Schlagal, Caitlin R., and Ping Wu. "Alcohol and Cocaine Combined Substance Use on Adult Hypothalamic Neural Stem Cells and Neurogenesis." Brain Plasticity 6, no. 1 (December 29, 2020): 41–46. http://dx.doi.org/10.3233/bpl-190091.

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Many advancements have been made over the years looking at the individual and combined effects of drugs of abuse on the brain, with one key area of research focusing on the effects on neurogenesis. An integral part of fetal brain development and, later, maintenance in the adult brain, neurogenesis occurs in three main regions: subventricularzone of the lateral ventricles (SVZ), subgranularzone of the dentate gyrus (SGZ), and the tanycyte layer in the hypothalamus (TL). We will review current literature on combined drugs of abuse and their effect on adult neurogenesis. More specifically, this review will focus on the effect of combining cocaine and alcohol. Additionally, the tanycyte layer will be explored in more depth and probed to look at the neurogenic properties of tanycytes and their role in neurogenesis.

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Marsili, Alessandro, Edith Sanchez, Praful Singru, John W. Harney, Ann Marie Zavacki, Ronald M. Lechan, and P. R. Larsen. "Thyroxine-induced expression of pyroglutamyl peptidase II and inhibition of TSH release precedes suppression of TRH mRNA and requires type 2 deiodinase." Journal of Endocrinology 211, no. 1 (July 25, 2011): 73–78. http://dx.doi.org/10.1530/joe-11-0248.

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Suppression of TSH release from the hypothyroid thyrotrophs is one of the most rapid effects of 3,3′,5′-triiodothyronine (T3) or thyroxine (T4). It is initiated within an hour, precedes the decrease in TSHβ mRNA inhibition and is blocked by inhibitors of mRNA or protein synthesis. TSH elevation in primary hypothyroidism requires both the loss of feedback inhibition by thyroid hormone in the thyrotrophs and the positive effects of TRH. Another event in this feedback regulation may be the thyroid hormone-mediated induction of the TRH-inactivating pyroglutamyl peptidase II (PPII) in the hypothalamic tanycytes. This study compared the chronology of the acute effects of T3 or T4 on TSH suppression, TRH mRNA in the hypothalamic paraventricular nucleus (PVN), and the induction of tanycyte PPII. In wild-type mice, T3 or T4 caused a 50% decrease in serum TSH in hypothyroid mice by 5 h. There was no change in TRH mRNA in PVN over this interval, but there was a significant increase in PPII mRNA in the tanycytes. In mice with genetic inactivation of the type 2 iodothyronine deiodinase, T3 decreased serum TSH and increased PPII mRNA levels, while T4-treatment was ineffective. We conclude that the rapid suppression of TSH in the hypothyroid mouse by T3 occurs prior to a decrease in TRH mRNA though TRH inactivation may be occurring in the median eminence through the rapid induction of tanycyte PPII. The effect of T4, but not T3, requires the type 2 iodothyronine deiodinase.

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Ceriani, Ricardo, and Kathleen E. Whitlock. "Gonadotropin Releasing Hormone (GnRH) Triggers Neurogenesis in the Hypothalamus of Adult Zebrafish." International Journal of Molecular Sciences 22, no. 11 (May 31, 2021): 5926. http://dx.doi.org/10.3390/ijms22115926.

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Recently, it has been shown in adult mammals that the hypothalamus can generate new cells in response to metabolic changes, and tanycytes, putative descendants of radial glia, can give rise to neurons. Previously we have shown in vitro that neurospheres generated from the hypothalamus of adult zebrafish show increased neurogenesis in response to exogenously applied hormones. To determine whether adult zebrafish have a hormone-responsive tanycyte-like population in the hypothalamus, we characterized proliferative domains within this region. Here we show that the parvocellular nucleus of the preoptic region (POA) labels with neurogenic/tanycyte markers vimentin, GFAP/Zrf1, and Sox2, but these cells are generally non-proliferative. In contrast, Sox2+ proliferative cells in the ventral POA did not express vimentin and GFAP/Zrf1. A subset of the Sox2+ cells co-localized with Fezf2:GFP, a transcription factor important for neuroendocrine cell specification. Exogenous treatments of GnRH and testosterone were assayed in vivo. While the testosterone-treated animals showed no significant changes in proliferation, the GnRH-treated animals showed significant increases in the number of BrdU-labeled cells and Sox2+ cells. Thus, cells in the proliferative domains of the zebrafish POA do not express radial glia (tanycyte) markers vimentin and GFAP/Zrf1, and yet, are responsive to exogenously applied GnRH treatment.

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Murphy, Michelle, and Francis J. P. Ebling. "The Role of Hypothalamic Tri-Iodothyronine Availability in Seasonal Regulation of Energy Balance and Body Weight." Journal of Thyroid Research 2011 (2011): 1–7. http://dx.doi.org/10.4061/2011/387562.

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Seasonal cycles of body weight provide a natural model system to understand the central control of energy balance. Studies of such cycles in Siberian hamsters suggest that a change in the hypothalamic availability of thyroid hormone is the key determinant of annual weight regulation. Uptake of thyroid hormone into the hypothalamus from the peripheral circulation occurs largely through a specific monocarboxylate transporter expressed by tanycyte cells lining the third ventricle. Tanycytes are the principal brain cell type expressing type II and type III deiodinases, so they control the local concentrations of T4, T3, and inactive metabolites. Type III deiodinase mRNA in tanycytes is photoperiodically upregulated in short photoperiod. This would be expected to reduce the availability of T3 in the hypothalamus by promoting the production of inactive metabolites such as rT3. Experimental microimplantation of T3 directly into the hypothalamus during short-days promotes a long-day phenotype by increasing food intake and body weight without affecting the peripheral thyroid axis. Thus, thyroid hormone exerts anabolic actions within the brain that play a key role in the seasonal regulation of body weight. Understanding the precise actions of thyroid hormone in the brain may identify novel targets for long-term pharmacological manipulation of body weight.

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Lewis, Jo E., John M. Brameld, Phil Hill, Dana Wilson, Perry Barrett, Francis J. P. Ebling, and Preeti H. Jethwa. "Thyroid hormone and vitamin D regulate VGF expression and promoter activity." Journal of Molecular Endocrinology 56, no. 2 (December 7, 2015): 123–34. http://dx.doi.org/10.1530/jme-15-0224.

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The Siberian hamster (Phodopus sungorus) survives winter by decreasing food intake and catabolizing abdominal fat reserves, resulting in a sustained, profound loss of body weight. Hypothalamic tanycytes are pivotal for this process. In these cells, short-winter photoperiods upregulate deiodinase 3, an enzyme that regulates thyroid hormone availability, and downregulate genes encoding components of retinoic acid (RA) uptake and signaling. The aim of the current studies was to identify mechanisms by which seasonal changes in thyroid hormone and RA signaling from tanycytes might ultimately regulate appetite and energy expenditure. proVGF is one of the most abundant peptides in the mammalian brain, and studies have suggested a role for VGF-derived peptides in the photoperiodic regulation of body weight in the Siberian hamster. In silico studies identified possible thyroid and vitamin D response elements in the VGF promoter. Using the human neuroblastoma SH-SY5Y cell line, we demonstrate that RA increases endogenous VGF expression (P<0.05) and VGF promoter activity (P<0.0001). Similarly, treatment with 1,25-dihydroxyvitamin D3 increased endogenous VGF mRNA expression (P<0.05) and VGF promoter activity (P<0.0001), whereas triiodothyronine (T3) decreased both (P<0.01 and P<0.0001). Finally, intra-hypothalamic administration of T3 blocked the short day-induced increase in VGF expression in the dorsomedial posterior arcuate nucleus of Siberian hamsters. Thus, we conclude that VGF expression is a likely target of photoperiod-induced changes in tanycyte-derived signals and is potentially a regulator of seasonal changes in appetite and energy expenditure.

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Sánchez, Edith, Miguel Angel Vargas, Praful S. Singru, Isel Pascual, Fidelia Romero, Csaba Fekete, Jean-Louis Charli, and Ronald M. Lechan. "Tanycyte Pyroglutamyl Peptidase II Contributes to Regulation of the Hypothalamic-Pituitary-Thyroid Axis through Glial-Axonal Associations in the Median Eminence." Endocrinology 150, no. 5 (January 29, 2009): 2283–91. http://dx.doi.org/10.1210/en.2008-1643.

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Pyroglutamyl peptidase II (PPII), a highly specific membrane-bound metallopeptidase that inactivates TRH in the extracellular space, is tightly regulated by thyroid hormone in cells of the anterior pituitary. Whether PPII has any role in the region where axons containing hypophysiotropic TRH terminate, the median eminence, is unknown. For this purpose, we analyzed the cellular localization and regulation of PPII mRNA in the mediobasal hypothalamus in adult, male rats. PPII mRNA was localized in cells lining the floor and infralateral walls of the third ventricle and coexpressed with vimentin, establishing these cells as tanycytes. PPII mRNA extended in a linear fashion from the tanycyte cell bodies in the base of the third ventricle to its cytoplasmic and end-feet processes in the external zone of the median eminence in close apposition to pro-TRH-containing axon terminals. Compared with vehicle-treated, euthyroid controls, animals made thyrotoxic by the ip administration of 10 μg l-T4 daily for 1–3 d, showed dramatically increased accumulation of silver grains in the mediobasal hypothalamus and an approximately 80% increase in enzymatic activity. PPII inhibition in mediobasal hypothalamic explants increased TRH secretion, whereas ip injection of a specific PPII inhibitor increased cold stress- and TRH-induced TSH levels in plasma. We propose that an increase in circulating thyroid hormone up-regulates PPII activity in tanycytes and enhances degradation of extracellular TRH in the median eminence through glial-axonal associations, contributing to the feedback regulation of thyroid hormone on anterior pituitary TSH secretion.

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Bolborea, Matei, Eric Pollatzek, Heather Benford, Tamara Sotelo-Hitschfeld, and Nicholas Dale. "Hypothalamic tanycytes generate acute hyperphagia through activation of the arcuate neuronal network." Proceedings of the National Academy of Sciences 117, no. 25 (June 8, 2020): 14473–81. http://dx.doi.org/10.1073/pnas.1919887117.

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Hypothalamic tanycytes are chemosensitive glial cells that contact the cerebrospinal fluid in the third ventricle and send processes into the hypothalamic parenchyma. To test whether they can activate neurons of the arcuate nucleus, we targeted expression of a Ca2+-permeable channelrhodopsin (CatCh) specifically to tanycytes. Activation of tanycytes ex vivo depolarized orexigenic (neuropeptide Y/agouti-related protein; NPY/AgRP) and anorexigenic (proopiomelanocortin; POMC) neurons via an ATP-dependent mechanism. In vivo, activation of tanycytes triggered acute hyperphagia only in the fed state during the inactive phase of the light–dark cycle.

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Sáenz de Miera, Cristina, Béatrice Bothorel, Catherine Jaeger, Valérie Simonneaux, and David Hazlerigg. "Maternal photoperiod programs hypothalamic thyroid status via the fetal pituitary gland." Proceedings of the National Academy of Sciences 114, no. 31 (July 17, 2017): 8408–13. http://dx.doi.org/10.1073/pnas.1702943114.

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In wild mammals, offspring development must anticipate forthcoming metabolic demands and opportunities. Within species, different developmental strategies may be used, dependent on when in the year conception takes place. This phenotypic flexibility is initiated before birth and is linked to the pattern of day length (photoperiod) exposure experienced by the mother during pregnancy. This programming depends on transplacental communication via the pineal hormone melatonin. Here, we show that, in the Siberian hamster (Phodopus sungorus), the programming effect of melatonin is mediated by the pars tuberalis (PT) of the fetal pituitary gland, before the fetal circadian system and autonomous melatonin production is established. Maternal melatonin acts on the fetal PT to control expression of thyroid hormone deiodinases in ependymal cells (tanycytes) of the fetal hypothalamus, and hence neuroendocrine output. This mechanism sets the trajectory of reproductive and metabolic development in pups and has a persistent effect on their subsequent sensitivity to the photoperiod. This programming effect depends on tanycyte sensitivity to thyroid stimulating hormone (TSH), which is dramatically and persistently increased by short photoperiod exposure in utero. Our results define the role of the fetal PT in developmental programming of brain function by maternal melatonin and establish TSH signal transduction as a key substrate for the encoding of internal calendar time from birth to puberty.

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Egri, P., C. Fekete, Á. Dénes, D. Reglődi, H. Hashimoto, B. D. Fülöp, and Balázs Gereben. "Pituitary Adenylate Cyclase-Activating Polypeptide (PACAP) Regulates the Hypothalamo-Pituitary-Thyroid (HPT) Axis via Type 2 Deiodinase in Male Mice." Endocrinology 157, no. 6 (April 5, 2016): 2356–66. http://dx.doi.org/10.1210/en.2016-1043.

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The hypothalamic activation of thyroid hormones by type 2 deiodinase (D2), catalyzing the conversion of thyroxine to T3, is critical for the proper function of the hypothalamo-pituitary-thyroid (HPT) axis. Regulation of D2 expression in tanycytes alters the activity of the HPT axis. However, signals that regulate D2 expression in tanycytes are poorly understood. The pituitary adenylate cyclase-activating polypeptide (PACAP) increases intracellular cAMP level, a second messenger known to stimulate the DIO2 gene; however, its importance in tanycytes is not completely characterized. Therefore, we tested whether this ubiquitously expressed neuropeptide regulates the HPT axis through stimulation of D2 in tanycytes. PACAP increased the activity of human DIO2 promoter in luciferase reporter assay that was abolished by mutation of cAMP-response element. Furthermore, PAC1R receptor immunoreactivity was identified in hypothalamic tanycytes, suggesting that these D2-expressing cells could be regulated by PACAP. Intracerebroventricular PACAP administration resulted in increased D2 activity in the mediobasal hypothalamus, suppressed Trh expression in the hypothalamic paraventricular nucleus, and decreased Tshb expression in the pituitary demonstrating that PACAP affects the D2-mediated control of the HPT axis. To understand the role of endogenous PACAP in the regulation of HPT axis, the effect of decreased PACAP expression was studied in heterozygous Adcyap1 (PACAP) knockout mice. These animals were hypothyroid that may be the consequence of altered hypothalamic T3 degradation during set-point formation of the HPT axis. In conclusion, PACAP is an endogenous regulator of the HPT axis by affecting T3-mediated negative feedback via cAMP-induced D2 expression of tanycytes.

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Balland, Églantine, and Vincent Prévot. "Les tanycytes hypothalamiques." médecine/sciences 30, no. 6-7 (June 2014): 624–27. http://dx.doi.org/10.1051/medsci/20143006009.

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Müller-Fielitz, Helge, and Markus Schwaninger. "The Role of Tanycytes in the Hypothalamus-Pituitary-Thyroid Axis and the Possibilities for Their Genetic Manipulation." Experimental and Clinical Endocrinology & Diabetes 128, no. 06/07 (December 11, 2019): 388–94. http://dx.doi.org/10.1055/a-1065-1855.

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AbstractThyroid hormone (TH) regulation is important for development, energy homeostasis, heart function, and bone formation. To control the effects of TH in target organs, the hypothalamus-pituitary-thyroid (HPT) axis and the tissue-specific availability of TH are highly regulated by negative feedback. To exert a central feedback, TH must enter the brain via specific transport mechanisms and cross the blood-brain barrier. Here, tanycytes, which are located in the ventral walls of the 3rd ventricle in the mediobasal hypothalamus (MBH), function as gatekeepers. Tanycytes are able to transport, sense, and modify the release of hormones of the HPT axis and are involved in feedback regulation. In this review, we focus on the relevance of tanycytes in thyrotropin-releasing hormone (TRH) release and review available genetic tools to investigate the physiological functions of these cells.

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Ebling, Francis J. P., and Ricardo Samms. "Txnip, Tanycytes, and Torpor." Endocrinology 154, no. 6 (June 1, 2013): 1970–72. http://dx.doi.org/10.1210/en.2013-1390.

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Osterstock, Guillaume, Taoufik El Yandouzi, Nicola Romanò, Danielle Carmignac, Fanny Langlet, Nathalie Coutry, Anne Guillou, et al. "Sustained Alterations of Hypothalamic Tanycytes During Posttraumatic Hypopituitarism in Male Mice." Endocrinology 155, no. 5 (May 1, 2014): 1887–98. http://dx.doi.org/10.1210/en.2013-1336.

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Traumatic brain injury is a leading cause of hypopituitarism, which compromises patients' recovery, quality of life, and life span. To date, there are no means other than standardized animal studies to provide insights into the mechanisms of posttraumatic hypopituitarism. We have found that GH levels were impaired after inducing a controlled cortical impact (CCI) in mice. Furthermore, GHRH stimulation enhanced GH to lower level in injured than in control or sham mice. Because many characteristics were unchanged in the pituitary glands of CCI mice, we looked for changes at the hypothalamic level. Hypertrophied astrocytes were seen both within the arcuate nucleus and the median eminence, two pivotal structures of the GH axis, spatially remote to the injury site. In the arcuate nucleus, GHRH neurons were unaltered. In the median eminence, injured mice exhibited unexpected alterations. First, the distributions of claudin-1 and zonula occludens-1 between tanycytes were disorganized, suggesting tight junction disruptions. Second, endogenous IgG was increased in the vicinity of the third ventricle, suggesting abnormal barrier properties after CCI. Third, intracerebroventricular injection of a fluorescent-dextran derivative highly stained the hypothalamic parenchyma only after CCI, demonstrating an increased permeability of the third ventricle edges. This alteration of the third ventricle might jeopardize the communication between the hypothalamus and the pituitary gland. In conclusion, the phenotype of CCI mice had similarities to the posttraumatic hypopituitarism seen in humans with intact pituitary gland and pituitary stalk. It is the first report of a pathological status in which tanycyte dysfunctions appear as a major acquired syndrome.

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Prager-Khoutorsky, Masha, and Charles W. Bourque. "Anatomical organization of the rat organum vasculosum laminae terminalis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 309, no. 4 (August 15, 2015): R324—R337. http://dx.doi.org/10.1152/ajpregu.00134.2015.

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The organum vasculosum of the laminae terminalis (OVLT) is a circumventricular organ located along the ventral part of the anterior wall of the third ventricle. Because it lacks a complete blood-brain barrier (BBB), blood-borne signals detected in the OVLT provide the brain with information from the periphery and contribute to the generation of centrally mediated responses to humoral feedback and physiological stressors. Experimental studies on the rat OVLT are hindered by a poor understanding of its precise anatomical dimensions and cellular organization. In this study, we use histological techniques to characterize the spatial outline of the rat OVLT and to examine the location of neurons, astrocytes, tanycytes, and ependymocytes within its confines. Our data reveal that OVLT neurons are embedded in a dense network of tanycyte processes. Immunostaining against the neuronal marker NeuN revealed that neurons are distributed throughout the OVLT, except for a thick midline septum, which comprises densely packed cells of unknown function or lineage. Moreover, the most ventral aspect of the OVLT is devoid of neurons and is occupied by a dense network of glial cell processes that form a thick layer between the neurons and the pial surface on the ventral aspect of the nucleus. Lastly, combined detection of NeuN and c-Fos protein following systemic injection of hypertonic NaCl revealed that neurons responsive to this stimulus are located along the entire midline core of the OVLT, extending from its most anterior ventral aspect to the more caudally located “dorsal cap” region.

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Sullivan, Andrew I., Matthew J. Potthoff, and Kyle H. Flippo. "Tany-Seq: Integrated Analysis of the Mouse Tanycyte Transcriptome." Cells 11, no. 9 (May 6, 2022): 1565. http://dx.doi.org/10.3390/cells11091565.

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The ability to maintain energy homeostasis is necessary for survival. Recently, an emerging role for ependymogial cells, which line the third ventricle in the hypothalamus in the regulation of energy homeostasis, has been appreciated. These cells are called tanycytes and are physically at the interface of brain communication with peripheral organs and have been proposed to mediate the transport of circulating hormones from the third ventricle into the parenchyma of the hypothalamus. Despite the important role tanycytes have been proposed to play in mediating communication from the periphery to the brain, we understand very little about the ontology and function of these cells due to their limited abundance and lack of ability to genetically target this cell population reliably. To overcome these hurdles, we integrated existing hypothalamic single cell RNA sequencing data, focusing on tanycytes, to allow for more in-depth characterization of tanycytic cell types and their putative functions. Overall, we expect this dataset to serve as a resource for the research community.

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Lazcano, Iván, Agustina Cabral, Rosa María Uribe, Lorraine Jaimes-Hoy, Mario Perello, Patricia Joseph-Bravo, Edith Sánchez-Jaramillo, and Jean-Louis Charli. "Fasting Enhances Pyroglutamyl Peptidase II Activity in Tanycytes of the Mediobasal Hypothalamus of Male Adult Rats." Endocrinology 156, no. 7 (May 5, 2015): 2713–23. http://dx.doi.org/10.1210/en.2014-1885.

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Fasting down-regulates the hypothalamus-pituitary-thyroid (HPT) axis activity through a reduction of TRH synthesis in neurons of the parvocellular paraventricular nucleus of the hypothalamus (PVN). These TRH neurons project to the median eminence (ME), where TRH terminals are close to the cytoplasmic extensions of β2 tanycytes. Tanycytes express pyroglutamyl peptidase II (PPII), the TRH-degrading ectoenzyme that controls the amount of TRH that reaches the anterior pituitary. We tested the hypothesis that regulation of ME PPII activity is another mechanism by which fasting affects the activity of the HPT axis. Semiquantitative in situ hybridization histochemistry data indicated that PPII and deiodinase 2 mRNA levels increased in tanycytes after 48 hours of fasting. This increase was transitory, followed by an increase of PPII activity in the ME, and a partial reversion of the reduction in PVN pro-TRH mRNA levels and the number of TRH neurons detected by immunohistochemistry. In fed animals, adrenalectomy and corticosterone treatment did not change ME PPII activity 72 hours later. Methimazole-induced hypothyroidism produced a profound drop in tanycytes PPII mRNA levels, which was reverted by 3 days of treatment with T4. The activity of thyroliberinase, the serum isoform of PPII, was increased at most fasting time points studied. We conclude that delayed increases in both the ME PPII as well as the thyroliberinase activities in fasted male rats may facilitate the maintenance of the deep down-regulation of the HPT axis function, despite a partial reactivation of TRH expression in the PVN.

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Elizondo-Vega, Roberto, Karina Oyarce, Magdiel Salgado, María José Barahona, Antonia Recabal, Patricio Ordenes, Sergio López, Roxana Pincheira, Patricia Luz-Crawford, and María Angeles García-Robles. "Inhibition of Hypothalamic MCT4 and MCT1–MCT4 Expressions Affects Food Intake and Alters Orexigenic and Anorexigenic Neuropeptide Expressions." Molecular Neurobiology 57, no. 2 (October 2, 2019): 896–909. http://dx.doi.org/10.1007/s12035-019-01776-6.

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Abstract Feeding behavior regulation is a complex process, which depends on the central integration of different signals, such as glucose, leptin, and ghrelin. Recent studies have shown that glial cells known as tanycytes that border the basal third ventricle (3V) detect glucose and then use glucose-derived signaling to inform energy status to arcuate nucleus (ARC) neurons to regulate feeding behavior. Monocarboxylate transporters (MCT) 1 and MCT4 are localized in the cellular processes of tanycytes, which could facilitate monocarboxylate release to orexigenic and anorexigenic neurons. We hypothesize that MCT1 and MCT4 inhibitions could alter the metabolic communication between tanycytes and ARC neurons, affecting feeding behavior. We have previously shown that MCT1 knockdown rats eat more and exhibit altered satiety parameters. Here, we generate MCT4 knockdown rats and MCT1–MCT4 double knockdown rats using adenovirus-mediated transduction of a shRNA into the 3V. Feeding behavior was evaluated in MCT4 and double knockdown animals, and neuropeptide expression in response to intracerebroventricular glucose administration was measured. MCT4 inhibition produced a decrease in food intake, contrary to double knockdown. MCT4 inhibition was accompanied by a decrease in eating rate and mean meal size and an increase in mean meal duration, parameters that are not changed in the double knockdown animals with exception of eating rate. Finally, we observed a loss in glucose regulation of orexigenic neuropeptides and abnormal expression of anorexigenic neuropeptides in response to fasting when these transporters are inhibited. Taken together, these results indicate that MCT1 and MCT4 expressions in tanycytes play a role in feeding behavior regulation.

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Bellamy, Charlotte, Hannah Tovell, Florent Dingli, Stephane Liva, Damarys Loew, Eduard Stefan, Selina Schwaighofer, Alexandra Newton, Marc Sanson, and Franck Bielle. "CSIG-30. FUNCTIONAL CHARACTERISATION OF A NOVEL MUTATION IN PRKCA, THE MAJOR DRIVER OF CHORDOID GLIOMAS." Neuro-Oncology 25, Supplement_5 (November 1, 2023): v47. http://dx.doi.org/10.1093/neuonc/noad179.0186.

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Abstract Chordoid gliomas (ChG) are a rare low-grade brain tumour, believed to be derived from Tanycytes. An analysis by the team previously identified a novel mutation present in all ChGs: PRKCA p.D463H. This mutation involves a D463H amino acid substitution at the kinase domain of the Protein kinase C alpha (PKCα) and represents the hallmark of ChG. PKCα is a serine/threonine kinase, that carries out the regulation of various functions in the cell. The aim of the project is to identify novel and biologically relevant PKCα D463H signalling pathways, which will demonstrate the involvement and the role of this mutated kinase in cellular functions implicated in the development of ChGs. The D463H mutation affects a critical residue of the kinase domain of PKCα, suggesting that such change may modify substrate affinity and specificity. Following the purification of the mutated form of PKCα, we have shown it is an inactive kinase, that has a dominant negative effect over the wild type (WT) PKCα. The mutation affects the tertiary structure of the protein, resulting in a more open, unstable protein. Phosphoproteomic analysis of HEK cells overexpressing the mutant protein has shown a global loss of PKCα substrate phosphosites compared to the WT condition. By understanding these changes, integrated with our snRNAseq and bulk RNAseq data of ChGs, we hope to elucidate the mechanism by which the mutation leads to tumorigenesis. Finally, the candidates will be explored in a representative context, by exploring the PKCɑ D463H mutation in primary rat Tanycyte culture and in vivo model. These models will allow us to study the effect of the mutation on cellular processes involved in the development of this rare tumour.

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Dale, Nicholas, and Cameron Frayling. "Tanycytes emerge as hypothalamic chemosensors." Physiology News, Spring 2012 (April 1, 2012): 26–29. http://dx.doi.org/10.36866/pn.86.26.

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Dietrich, Marcelo O., and Tamas L. Horvath. "Fat incites tanycytes to neurogenesis." Nature Neuroscience 15, no. 5 (April 25, 2012): 651–53. http://dx.doi.org/10.1038/nn.3091.

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Frayling, Cameron, Ruth Britton, and Nicholas Dale. "ATP-mediated glucosensing by hypothalamic tanycytes." Journal of Physiology 589, no. 9 (April 27, 2011): 2275–86. http://dx.doi.org/10.1113/jphysiol.2010.202051.

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Gao, Yuanqing, Matthias H. Tschöp, and Serge Luquet. "Hypothalamic Tanycytes: Gatekeepers to Metabolic Control." Cell Metabolism 19, no. 2 (February 2014): 173–75. http://dx.doi.org/10.1016/j.cmet.2014.01.008.

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Severi, Ilenia, Marco Fosca, Georgia Colleluori, Federico Marini, Luca Imperatori, Martina Senzacqua, Angelica Di Vincenzo, et al. "High-Fat Diet Impairs Mouse Median Eminence: A Study by Transmission and Scanning Electron Microscopy Coupled with Raman Spectroscopy." International Journal of Molecular Sciences 22, no. 15 (July 28, 2021): 8049. http://dx.doi.org/10.3390/ijms22158049.

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Hypothalamic dysfunction is an initial event following diet-induced obesity, primarily involving areas regulating energy balance such as arcuate nucleus (Arc) and median eminence (ME). To gain insights into the early hypothalamic diet-induced alterations, adult CD1 mice fed a high-fat diet (HFD) for 6 weeks were studied and compared with normo-fed controls. Transmission and scanning electron microscopy and histological staining were employed for morphological studies of the ME, while Raman spectroscopy was applied for the biochemical analysis of the Arc-ME complex. In HFD mice, ME β2-tanycytes, glial cells dedicated to blood-liquor crosstalk, exhibited remarkable ultrastructural anomalies, including altered alignment, reduced junctions, degenerating organelles, and higher content of lipid droplets, lysosomes, and autophagosomes. Degenerating tanycytes also displayed an electron transparent cytoplasm filled with numerous vesicles, and they were surrounded by dilated extracellular spaces extending up to the subependymal layer. Consistently, Raman spectroscopy analysis of the Arc-ME complex revealed higher glycogen, collagen, and lipid bands in HFD mice compared with controls, and there was also a higher band corresponding to the cyanide group in the former compared to the last. Collectively, these data show that ME β2-tanycytes exhibit early structural and chemical alterations due to HFD and reveal for the first-time hypothalamic cyanide presence following high dietary lipids consumption, which is a novel aspect with potential implications in the field of obesity.

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Prévot, Vincent. "Brain infection by SARS-CoV-2: Lifelong consequences." Open Access Government 41, no. 1 (January 23, 2024): 22–23. http://dx.doi.org/10.56367/oag-041-10397.

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Brain infection by SARS-CoV-2: Lifelong consequences The WATCH team, founded to elucidate the role played by specialized brain cells called tanycytes in various physiological processes, has been investigating how and where the SARS-CoV-2 virus infects the brain, and some long-term consequences of this neuro-invasion. The European Research Council (ERC) Synergy project WATCH (Well-Aging and the Tanycytic Control of Health) brings together the teams of three principal investigators: Vincent Prevot, a neuroendocrinologist working for the French National Health Research Institute (INSERM) in Lille, France; Markus Schwaninger, a neurologist at the University of Lübeck, Germany; and Ruben Nogueiras, an expert in molecular metabolism at the University of Santiago de Compostela in Spain. Together, they are researching how tanycytes – highly specialized cells residing in a tiny part of the brain called the hypothalamus – regulate various physiological processes.

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Przybylska-Piech, Anna S., Victoria Diedrich, and Annika Herwig. "Seasonal changes in activity of hypothalamic thyroid hormone system in different winter phenotypes of Djungarian hamster (Phodopus sungorus)." PLOS ONE 19, no. 10 (October 25, 2024): e0309591. http://dx.doi.org/10.1371/journal.pone.0309591.

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Although the Djungarian hamster (Phodopus sungorus) is a seasonality model, it presents substantial variability in winter acclimation. In response to short photoperiod, some individuals express a suite of winter traits such as low body mass, regressed gonads, white fur, and daily torpor, while others develop only some adjustments or maintain a summer phenotype. Despite comprehensive research, the mechanisms underlying polymorphism of winter phenotype are still unknown. We compared key elements of the hypothalamic thyroid hormone system, as well as the tanycyte architecture in hamsters of both sexes. Individuals presented different responses to short photoperiod characterized either as phenotypes (non-responder, partial-responder and full-responder) or photoresponsive index. We measured the expression of genes coding iodothyronine deiodinase 2 and 3, monocarboxylate transporter 8, thyrotropin-releasing hormone, and somatostatin in 40 individuals and counted the number of immunolabeled tanycyte processes in standardized regions of interest around the third ventricle in 30 individuals. Animals acclimated to short photoperiod presented a downregulation of diodinase 2 and somatostatin and an upregulation of deiodinase 3, as well as a decreased number of tanycyte processes, compared to long photoperiod-exposed individuals. Although phenotypes did not differ in gene expression, the higher the photoresponsive index, the lower was the deiodinase 2 expression and the higher the deiodinase 3 expression. Partial-responders and full-responders had less tanycyte processes than non-responders, and the number of tanycyte processes correlated with the photoresponsive index. Sexes differed neither in their seasonal response, nor hypothalamic gene expression, but females had more tanycyte processes. Our results are in accordance with studies emphasizing the pivotal role of thyroid hormones in seasonal response. We suggest that the whole spectrum of winter phenotypes exists within the population of Djungarian hamsters and that it is reflected also at the level of neuroendocrine regulation. However, the neuroendocrine underpinnings of winter phenotype polymorphism require further investigation.

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Prevot, Vincent, Markus Schwaninger, and Ruben Nogueiras. "The WATCH project: Tanycytes in health and disease." Open Access Government 37, no. 1 (January 6, 2023): 132–33. http://dx.doi.org/10.56367/oag-037-10410.

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The WATCH project: Tanycytes in health and disease In our aging societies, maintaining health and limiting age-related metabolic or cognitive disorders are of primordial importance not only for the well-being of the individual but also from the economic and societal points of view. The Synergy project Well-Aging and the Tanycytic Control of Health (WATCH), funded by the European Research Council (ERC), is a high-impact project conducted by Vincent Prévot, a neuroendocrinologist working for the French national health research institute (Inserm), in Lille, France; Markus Schwaninger, a neurologist at the University of Lübeck, Germany; and Ruben Nogueiras, an expert in molecular metabolism at the University of Santiago de Compostela in Spain. Together, these three teams aim to understand how a small and highly specialized population of brain cells called tanycytes regulate a variety of physiological processes, and the implications of their function or dysfunction for healthy aging.

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Givalois, Laurent, Sandor Arancibia, Gérard Alonso, and Lucia Tapia-Arancibia. "Expression of Brain-Derived Neurotrophic Factor and Its Receptors in the Median Eminence Cells with Sensitivity to Stress." Endocrinology 145, no. 10 (October 1, 2004): 4737–47. http://dx.doi.org/10.1210/en.2004-0616.

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Abstract The median eminence (ME) is considered as the final common pathway connecting the nervous and endocrine systems. In this neurohemal structure, dynamic interactions among nerve terminals, tanycytes, and astrocytes determine through plastic processes the neurohormones access to the portal blood. Because brain-derived neurotrophic factor (BDNF) is involved in plastic changes, we investigated its presence and that of its receptors (TrkB) in the different cellular types described in the ME. Using in situ hybridization and immunohistochemical techniques, we demonstrated that BDNF immunoreactivity was essentially located in the astrocytes and to a lesser extent in tanycytes. By contrast, BDNF was not detected in nerve terminals reaching the external layer of the ME. TrkB antibodies recognizing the extracellular receptor domain labeled all of these different cell types, suggesting an autocrine or paracrine action of BDNF at this level. More selective antibodies showed that TrkB.FL immunostaining was found in tanycytes and nerve endings, whereas TrkB.T1 immunostaining was localized in all cellular types. Immobilization stress increased BDNF mRNA and BDNF immunoreactivity patterns and induced biphasic BDNF release from the ME, as analyzed by push-pull perfusion. In addition, we observed that 60-min stress intensified BDNF immunoreactivity in the internal layer and also its colocalization with glial fibrillary acidic protein. Stress also accentuated BDNF immunostaining in the perivascular space in elements that were not labeled with antibodies recognizing fibroblast or endothelial cells. These data disclosed a novel location of BDNF and its receptors in the ME, which are presumably involved in dynamic processes such as hormone release.

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Langlet, F. "Tanycytes: A Gateway to the Metabolic Hypothalamus." Journal of Neuroendocrinology 26, no. 11 (October 16, 2014): 753–60. http://dx.doi.org/10.1111/jne.12191.

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Elizondo‐Vega, Roberto, Christian Cortes‐Campos, Maria J. Barahona, Karina A. Oyarce, Claudio A. Carril, and Maria A. García‐Robles. "The role of tanycytes in hypothalamic glucosensing." Journal of Cellular and Molecular Medicine 19, no. 7 (June 17, 2015): 1471–82. http://dx.doi.org/10.1111/jcmm.12590.

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Langlet, Fanny. "Targeting Tanycytes: Balance between Efficiency and Specificity." Neuroendocrinology 110, no. 7-8 (2020): 574–81. http://dx.doi.org/10.1159/000505549.

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Ebling, Francis J. P., and Jo E. Lewis. "Tanycytes and hypothalamic control of energy metabolism." Glia 66, no. 6 (February 7, 2018): 1176–84. http://dx.doi.org/10.1002/glia.23303.

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Dardente, Hugues. "HYPOTHALAMIC TANYCYTES ARE INVOLVED IN SEASONAL FUNCTIONS." IBRO Neuroscience Reports 15 (October 2023): S52. http://dx.doi.org/10.1016/j.ibneur.2023.08.2159.

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de Vries, E. M., S. Nagel, R. Haenold, S. M. Sundaram, F. W. Pfrieger, E. Fliers, H. Heuer, and A. Boelen. "The Role of Hypothalamic NF-κB Signaling in the Response of the HPT-Axis to Acute Inflammation in Female Mice." Endocrinology 157, no. 7 (May 17, 2016): 2947–56. http://dx.doi.org/10.1210/en.2016-1027.

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A large proportion of critically ill patients have alterations in the hypothalamus-pituitary-thyroid (HPT) axis, collectively known as the nonthyroidal illness syndrome. Nonthyroidal illness syndrome is characterized by low serum thyroid hormone (TH) concentrations accompanied by a suppressed central component of the HPT axis and persistent low serum TSH. In hypothalamic tanycytes, the expression of type 2 deiodinase (D2) is increased in several animal models of inflammation. Because D2 is a major source of T3 in the brain, this response is thought to suppress TRH expression in the paraventricular nucleus via increased local bioavailability of T3. The inflammatory pathway component RelA (the p65 subunit of nuclear factor-κB) can bind the Dio2 promoter and increases D2 expression after lipopolysaccharide (LPS) stimulation in vitro. We aimed to determine whether RelA signaling in tanycytes is essential for the LPS-induced D2 increase in vivo by conditional elimination of RelA in tanycytes of mice (RelAASTKO). Dio2 and Trh mRNA expression were assessed by quantitative in situ hybridization 8 or 24 hours after saline or LPS injection. At the same time points, we measured pituitary Tshβ mRNA expression and serum T3 and T4 concentrations. In RelAASTKO mice the LPS-induced increase in Dio2 and decrease in Trh mRNA levels in the hypothalamus were reduced compared with the wild-type littermates, whereas the drop in pituitary Tshβ expression and in serum TH concentrations persisted. In conclusion, RelA is essential for the LPS-induced hypothalamic D2 increase and TRH decrease. The central changes in the HPT axis are, however, not required for the down-regulation of Tshβ expression and serum TH concentrations.

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Barahona, María Jose, Luciano Ferrada, and Francisco Nualart. "TANYCYTES-ASSOCIATED G6PASE SYSTEM CONTROL THE ENERGY BALANCE." IBRO Neuroscience Reports 15 (October 2023): S213. http://dx.doi.org/10.1016/j.ibneur.2023.08.340.

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Bjelke, Börje, and Kjell Fuxe. "Intraventricular β-endorphin accumulates in DARPP-32 immunoreactive tanycytes." NeuroReport 5, no. 3 (December 1993): 265–68. http://dx.doi.org/10.1097/00001756-199312000-00021.

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Böttcher, Mareike, Helge Müller-Fielitz, Sivaraj M. Sundaram, Sarah Gallet, Vanessa Neve, Kiseko Shionoya, Adriano Zager, et al. "NF-κB signaling in tanycytes mediates inflammation-induced anorexia." Molecular Metabolism 39 (September 2020): 101022. http://dx.doi.org/10.1016/j.molmet.2020.101022.

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Dale, Nicholas. "Purinergic signaling in hypothalamic tanycytes: Potential roles in chemosensing." Seminars in Cell & Developmental Biology 22, no. 2 (April 2011): 237–44. http://dx.doi.org/10.1016/j.semcdb.2011.02.024.

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RODRIGUEZ, E., J. BLAZQUEZ, F. PASTOR, B. PELAEZ, P. PENA, B. PERUZZO, and P. AMAT. "Hypothalamic Tanycytes: A Key Component of Brain–Endocrine Interaction." International Review of Cytology 247 (2005): 89–164. http://dx.doi.org/10.1016/s0074-7696(05)47003-5.

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Cup�do, R. N. J., and H. Weerd. "Tanycytes in the medial habenular nucleus of the rat." Anatomy and Embryology 172, no. 1 (June 1985): 7–10. http://dx.doi.org/10.1007/bf00318938.

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Rivagorda, Manon, Vincent Prevot, and Markus Schwaninger. "Seasonal biology: Tanycytes give the hypothalamus a spring makeover." Current Biology 34, no. 5 (March 2024): R209—R211. http://dx.doi.org/10.1016/j.cub.2024.01.055.

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Journal articles on the topic 'Tanyctes'

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