The Experts below are selected from a list of 240 Experts worldwide ranked by ideXlab platform

Vincent Prevot - One of the best experts on this subject based on the ideXlab platform.

  • tanycytes in the infundibular nucleus and Median Eminence and their role in the blood brain barrier
    Handbook of Clinical Neurology, 2021
    Co-Authors: Vincent Prevot, Ruben Nogueiras, Markus Schwaninger
    Abstract:

    The blood-brain barrier is generally attributed to endothelial cells. However, in circumventricular organs, such as the Median Eminence, tanycytes take over the barrier function. These ependymoglial cells form the wall of the third ventricle and send long extensions into the parenchyma to contact blood vessels and hypothalamic neurons. The shape and location of tanycytes put them in an ideal position to connect the periphery with central nervous compartments. In line with this, tanycytes control the transport of hormones and key metabolites in and out of the hypothalamus. They function as sensors of peripheral homeostasis for central regulatory networks. This chapter discusses current evidence that tanycytes play a key role in regulating glucose balance, food intake, endocrine axes, seasonal changes, reproductive function, and aging. The understanding of how tanycytes perform these diverse tasks is only just beginning to emerge and will probably lead to a more differentiated view of how the brain and the periphery interact.

  • Gonadotrophin-releasing hormone nerve terminals, tanycytes and neurohaemal junction remodelling in the adult Median Eminence: functional consequences for reproduction and dynamic role of vascular endothelial cells.
    Journal of Neuroendocrinology, 2010
    Co-Authors: Vincent Prevot, Jyoti Parkash, Nicole Bellefontaine, Marc Baroncini, Ariane Sharif, Naresh Kumar Hanchate, Céline Campagne, Sandrine De Seranno
    Abstract:

    Although coordinated actions of several areas within the hypothalamus are involved in the secretion of gonadotrophin-releasing hormone (GnRH), the Median Eminence of the hypothalamus, where the nerve terminals are located, plays a particularly critical role in the release of GnRH. In adult females, prior to the preovulatory surge of GnRH, the retraction of specialised ependymoglial cells lining the floor of the third ventricle named tanycytes allows for the juxtaposition of GnRH nerve terminals with the adjacent pericapillary space of the pituitary portal vasculature, thus forming direct neurohaemal junctions. These morphological changes occur within a few hours and are reversible. Such remodelling may promote physiological conditions to enhance the central release of GnRH and potentiate oestrogen-activated GnRH release. This plasticity involves dynamic cell interactions that bring into play tanycytes, astrocytes, vascular endothelial cells and GnRH neurones themselves. The underlying signalling pathways responsible for these structural changes are comprised of highly diffusible gaseous molecules, such as endothelial nitric oxide, and paracrine communication processes involving receptors of the erbB tyrosine kinase family, transforming growth factor beta 1 and eicosanoids, such as prostaglandin E(2). Some of these molecules, as a result of their ability to diffuse within the Median Eminence, may also serve as synchronizing cues allowing for the occurrence of functionally meaningful episodes of GnRH secretion by coordinating GnRH release from the GnRH neuroendocrine terminals.

  • Role of estradiol in the dynamic control of tanycyte plasticity mediated by vascular endothelial cells in the Median Eminence.
    Endocrinology, 2010
    Co-Authors: Sandrine De Seranno, Xavier D'anglemont De Tassigny, Cecilia Estrella, Anne Loyens, Sergey Kasparov, Danièle Leroy, Sergio R. Ojeda, J.c. Beauvillain, Vincent Prevot
    Abstract:

    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-E(2) (PGE(2)) 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 PGE(2) to Median Eminence explants induces rapid neuroglial plasticity at the neurovascular junction of neurons that release GnRH (the neuropeptide controlling reproduction). Conversely, preventing local PGE(2) 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.

  • variation of endothelial nitric oxide synthase synthesis in the Median Eminence during the rat estrous cycle an additional argument for the implication of vascular blood vessel in the control of gnrh release
    Endocrinology, 2001
    Co-Authors: Claude Knauf, Vincent Prevot, Jeanclaude Beauvillain, Stephanie Ferreira, Malika Hamdane, Christel Mailliot, Dominique Croix
    Abstract:

    Recent studies from our laboratory suggested that the vascular endothelium of the Median Eminence was involved via nitric oxide secretion in the modulation of GnRH release during the estrous cycle. To further investigate that issue, we studied the variations of endothelial nitric oxide synthase protein and mRNA in the Median Eminence of female rats killed at different time points of the day and/or of the estrous cycle. Endothelial nitric oxide synthase protein levels were measured by Western blot, and endothelial nitric oxide synthase mRNA analysis was performed with semiquantitative RT-PCR (for each time point, n = 4). The results revealed that endothelial nitric oxide synthase synthesis varied markedly across the estrous cycle. Indeed, endothelial nitric oxide synthase protein (n = 20) and mRNA (n = 16) levels increase significantly on 0800 h and 1600 h proestrus compared with 1400 h diestrus II. In a second step, quantification analysis were made in Median Eminence obtained from ovariectomized and ovariectomized, E2 benzoate primed rat. The results show a significant increase in expression of endothelial nitric oxide synthase protein as well as endothelial nitric oxide synthase mRNA in ovx-E2 primed rat Median Eminence. Concurrently, the levels of the cav-1 protein, a specific endogenous inhibitor of endothelial nitric oxide synthase, were measured in Median Eminence during estrous cycle and in ME from ovx and ovx-E2 primed rats. A significant decrease of Median Eminence cav-1 was noted on 1600 h proestrus and in ovx-E2 primed rats when compared with 1400 h diestrus II and ovx, respectively. Altogether, these results strongly suggest that high NO release from Median Eminence observed on proestrus may be due to an increase of endothelial nitric oxide synthase expression and a decrease of the cav-1 protein levels. These findings demonstrate that E2 is able to modulate endothelial nitric oxide synthase and cav-1 expression both during the estrous cycle and in experimental conditions and consequently reinforce the idea that nitric oxide acting on GnRH release, is essentially endothelial in origin. These results may also imply that variations of endothelial nitric oxide synthase expression are essential for the pulsatile/cyclic nitric oxide Median Eminence release observed in a previous study.

  • evidence for a spontaneous nitric oxide release from the rat Median Eminence influence on gonadotropin releasing hormone release
    Endocrinology, 2001
    Co-Authors: Claude Knauf, Vincent Prevot, Jeanclaude Beauvillain, George B Stefano, Genevieve Mortreux, Dominique Croix
    Abstract:

    The involvement of nitric oxide (NO) as a gaseous neurotransmitter in the hypothalamic control of pituitary LH secretion has been demonstrated. NO, as a diffusible signaling gas, has the ability to control and synchronize the activity of the neighboring cells. NO is secreted at the Median Eminence (ME), the common termination field for the antehypophysiotropic neurons, under the stimulation of other signaling substances. At the ME, NO stimulates GnRH release from neuroendocrine terminals. The present studies were undertaken to determine whether NO is secreted spontaneously from ME fragments ex vivo and whether its secretion is correlated to GnRH release. To accomplish this, female rats were killed at different time points of the day and/or of the estrous cycle. The spontaneous NO release was monitored in real time, with an amperometric probe, during 4 periods of 30 min, from individual ME fragments (for each time point, n = 4). GnRH levels were measured in parallel for each incubation-period by RIA. The r...

Sandrine De Seranno - One of the best experts on this subject based on the ideXlab platform.

  • Gonadotrophin-releasing hormone nerve terminals, tanycytes and neurohaemal junction remodelling in the adult Median Eminence: functional consequences for reproduction and dynamic role of vascular endothelial cells.
    Journal of Neuroendocrinology, 2010
    Co-Authors: Vincent Prevot, Jyoti Parkash, Nicole Bellefontaine, Marc Baroncini, Ariane Sharif, Naresh Kumar Hanchate, Céline Campagne, Sandrine De Seranno
    Abstract:

    Although coordinated actions of several areas within the hypothalamus are involved in the secretion of gonadotrophin-releasing hormone (GnRH), the Median Eminence of the hypothalamus, where the nerve terminals are located, plays a particularly critical role in the release of GnRH. In adult females, prior to the preovulatory surge of GnRH, the retraction of specialised ependymoglial cells lining the floor of the third ventricle named tanycytes allows for the juxtaposition of GnRH nerve terminals with the adjacent pericapillary space of the pituitary portal vasculature, thus forming direct neurohaemal junctions. These morphological changes occur within a few hours and are reversible. Such remodelling may promote physiological conditions to enhance the central release of GnRH and potentiate oestrogen-activated GnRH release. This plasticity involves dynamic cell interactions that bring into play tanycytes, astrocytes, vascular endothelial cells and GnRH neurones themselves. The underlying signalling pathways responsible for these structural changes are comprised of highly diffusible gaseous molecules, such as endothelial nitric oxide, and paracrine communication processes involving receptors of the erbB tyrosine kinase family, transforming growth factor beta 1 and eicosanoids, such as prostaglandin E(2). Some of these molecules, as a result of their ability to diffuse within the Median Eminence, may also serve as synchronizing cues allowing for the occurrence of functionally meaningful episodes of GnRH secretion by coordinating GnRH release from the GnRH neuroendocrine terminals.

  • Role of estradiol in the dynamic control of tanycyte plasticity mediated by vascular endothelial cells in the Median Eminence.
    Endocrinology, 2010
    Co-Authors: Sandrine De Seranno, Xavier D'anglemont De Tassigny, Cecilia Estrella, Anne Loyens, Sergey Kasparov, Danièle Leroy, Sergio R. Ojeda, J.c. Beauvillain, Vincent Prevot
    Abstract:

    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-E(2) (PGE(2)) 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 PGE(2) to Median Eminence explants induces rapid neuroglial plasticity at the neurovascular junction of neurons that release GnRH (the neuropeptide controlling reproduction). Conversely, preventing local PGE(2) 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.

Ronald M Lechan - One of the best experts on this subject based on the ideXlab platform.

  • tanycyte pyroglutamyl peptidase ii contributes to regulation of the hypothalamic pituitary thyroid axis through glial axonal associations in the Median Eminence
    Endocrinology, 2009
    Co-Authors: Edith Sanchez, Ronald M Lechan, Miguel Angel Vargas, Praful S Singru, Isel Pascual, Fidelia Romero, Csaba Fekete, Jeanlouis Charli
    Abstract:

    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.

J.c. Beauvillain - One of the best experts on this subject based on the ideXlab platform.

  • Role of estradiol in the dynamic control of tanycyte plasticity mediated by vascular endothelial cells in the Median Eminence.
    Endocrinology, 2010
    Co-Authors: Sandrine De Seranno, Xavier D'anglemont De Tassigny, Cecilia Estrella, Anne Loyens, Sergey Kasparov, Danièle Leroy, Sergio R. Ojeda, J.c. Beauvillain, Vincent Prevot
    Abstract:

    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-E(2) (PGE(2)) 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 PGE(2) to Median Eminence explants induces rapid neuroglial plasticity at the neurovascular junction of neurons that release GnRH (the neuropeptide controlling reproduction). Conversely, preventing local PGE(2) 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.

  • definitive evidence for the existence of morphological plasticity in the external zone of the Median Eminence during the rat estrous cycle implication of neuro glio endothelial interactions in gonadotropin releasing hormone release
    Neuroscience, 1999
    Co-Authors: Vincent Prevot, Dominique Croix, George B Stefano, Sebastien G Bouret, S Dutoit, G Tramu, J.c. Beauvillain
    Abstract:

    Despite intense investigation, the demonstration of morphological plasticity in the external zone of the Median Eminence concerning the gonadotropin-releasing hormone system has never been reported. In this study, we investigate whether dynamic transformations of the gonadotropin-releasing hormone nerve terminals and/or tanycytes in the external zone of the Median Eminence of the hypothalamus occurred during the rat estrous cycle, by following individual gonadotropin-releasing hormone-immunoreactive nerve terminals on serial ultrathin sections observed by electron microscopy. Female rats were killed at 16.00 diestrus II (n=3), i.e. when estrogen levels are basal and gonadotropin-releasing hormone release is low, and at 16.00 proestrus (n=4), i.e. when estrogen levels peak and the preovulatory gonadotropin-releasing hormone surge occurs. Our results show that, in the Median Eminence obtained from proestrus rats, 12±2% of the gonadotropin-releasing hormone nerve terminals were observed to make physical contact with the parenchymatous basal lamina, i.e. the pericapillary space. In the Median Eminence obtained from diestrus II rats, no contacts were observed. On proestrus, numerous physical contacts between gonadotropin-releasing hormone nerve terminals and the basal lamina occurred by evagination of the basal lamina and/or by emerging processes from gonadotropin-releasing hormone nerve terminals. The quantification of the evagination of the basal lamina revealed that the basal lamina was at least twofold more tortuous in appearance during proestrus. These results demonstrate for the first time the existence of dynamic plastic changes in the external zone of the Median Eminence, allowing gonadotropin-releasing hormone nerve terminals to contact the pericapillary space on the day of proestrus, thus facilitating the release of the neurohormone into the pituitary portal blood.

Eliana P Araujo - One of the best experts on this subject based on the ideXlab platform.

  • dietary fats promote functional and structural changes in the Median Eminence blood spinal fluid interface the protective role for bdnf
    Journal of Neuroinflammation, 2018
    Co-Authors: Albina F Ramalho, Bruna Bombassaro, Nathalia Romanelli Vicente Dragano, Carina Solon, Joseane Morari, Milena Fioravante, Roberta Barbizan, Licio A Velloso, Eliana P Araujo
    Abstract:

    The consumption of large amounts of dietary fats activates an inflammatory response in the hypothalamus, damaging key neurons involved in the regulation of caloric intake and energy expenditure. It is currently unknown why the mediobasal hypothalamus is the main target of diet-induced brain inflammation. We hypothesized that dietary fats can damage the Median Eminence blood/spinal fluid interface. Swiss mice were fed on a high-fat diet, and molecular and structural studies were performed employing real-time PCR, immunoblot, immunofluorescence, transmission electron microscopy, and metabolic measurements. The consumption of a high fat diet was sufficient to increase the expression of inflammatory cytokines and brain-derived neurotrophic factor in the Median Eminence, preceding changes in other circumventricular regions. In addition, it led to an early loss of the structural organization of the Median Eminence β1-tanycytes. This was accompanied by an increase in the hypothalamic expression of brain-derived neurotrophic factor. The immunoneutralization of brain-derived neurotrophic factor worsened diet-induced functional damage of the Median Eminence blood/spinal fluid interface, increased diet-induced hypothalamic inflammation, and increased body mass gain. The Median Eminence/spinal fluid interface is affected at the functional and structural levels early after introduction of a high-fat diet. Brain-derived neurotrophic factor provides an early protection against damage, which is lost upon a persisting consumption of large amounts of dietary fats.

  • Dietary fats promote functional and structural changes in the Median Eminence blood/spinal fluid interface—the protective role for BDNF
    BMC, 2018
    Co-Authors: Albina F Ramalho, Bruna Bombassaro, Nathalia Romanelli Vicente Dragano, Carina Solon, Joseane Morari, Milena Fioravante, Roberta Barbizan, Licio A Velloso, Eliana P Araujo
    Abstract:

    Abstract Background The consumption of large amounts of dietary fats activates an inflammatory response in the hypothalamus, damaging key neurons involved in the regulation of caloric intake and energy expenditure. It is currently unknown why the mediobasal hypothalamus is the main target of diet-induced brain inflammation. We hypothesized that dietary fats can damage the Median Eminence blood/spinal fluid interface. Methods Swiss mice were fed on a high-fat diet, and molecular and structural studies were performed employing real-time PCR, immunoblot, immunofluorescence, transmission electron microscopy, and metabolic measurements. Results The consumption of a high fat diet was sufficient to increase the expression of inflammatory cytokines and brain-derived neurotrophic factor in the Median Eminence, preceding changes in other circumventricular regions. In addition, it led to an early loss of the structural organization of the Median Eminence β1-tanycytes. This was accompanied by an increase in the hypothalamic expression of brain-derived neurotrophic factor. The immunoneutralization of brain-derived neurotrophic factor worsened diet-induced functional damage of the Median Eminence blood/spinal fluid interface, increased diet-induced hypothalamic inflammation, and increased body mass gain. Conclusions The Median Eminence/spinal fluid interface is affected at the functional and structural levels early after introduction of a high-fat diet. Brain-derived neurotrophic factor provides an early protection against damage, which is lost upon a persisting consumption of large amounts of dietary fats