Vascular Endothelial Cells Promote Acute Plasticity in Ependymoglial Cells of the Neuroendocrine Brain

Seranno, Sandrine De; Estrella, Cecilia; Loyens, Anne; Cornea, Anda; Ojeda, Sergio R.; Beauvillain, Jean Claude; Prévot, Vincent

doi:10.1523/jneurosci.3228-04.2004

Cited by 72 publications

(100 citation statements)

References 57 publications

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“…In addition to modulating GnRH neuronal activity within the preoptic region, accumulating evidence suggests that NO is involved in the control of GnRH release within the median eminence, the termination field of GnRH neuroendocrine neurons (Rettori et al, 1993;Knauf et al, 2001;de Seranno et al, 2004de Seranno et al, , 2010, and another brain site that lies outside of the blood-brain barrier (Ciofi et al, 2009;Mullier et al, 2010). Because kisspeptin has also been shown to stimulate GnRH release from hypothalamic explants containing both the median eminence and the ARH (d'Anglemont de , and because arcuate nNOS neurons reside adjacent to the median eminence (Sica et al, 2009), one could argue that a part of the effects observed on LH secretion after the systemic administration of kisspeptin and Figure 9.…”

Section: Discussionmentioning

confidence: 99%

Kisspeptin-GPR54 Signaling in Mouse NO-Synthesizing Neurons Participates in the Hypothalamic Control of Ovulation

Parkash²,

et al. 2012

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Reproduction is controlled in the brain by a neural network that drives the secretion of gonadotropin-releasing hormone (GnRH).Various permissive homeostatic signals must be integrated to achieve ovulation in mammals. However, the neural events controlling the timely activation of GnRH neurons are not completely understood. Here we show that kisspeptin, a potent activator of GnRH neuronal activity, directly communicates with neurons that synthesize the gaseous transmitter nitric oxide (NO) in the preoptic region to coordinate the progression of the ovarian cycle. Using a transgenic Gpr54-null IRES-LacZ knock-in mouse model, we demonstrate that neurons containing neuronal NO synthase (nNOS), which are morphologically associated with kisspeptin fibers, express the kisspeptin receptor GPR54 in the preoptic region, but not in the tuberal region of the hypothalamus. The activation of kisspeptin signaling in preoptic neurons promotes the activation of nNOS through its phosphorylation on serine 1412 via the AKT pathway and mimics the positive feedback effects of estrogens. Finally, we show that while NO release restrains the reproductive axis at stages of the ovarian cycle during which estrogens exert their inhibitory feedback, it is required for the kisspeptin-dependent preovulatory activation of GnRH neurons. Thus, interactions between kisspeptin and nNOS neurons may play a central role in regulating the hypothalamic-pituitary-gonadal axis in vivo.

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Section: Discussionmentioning

confidence: 99%

Kisspeptin-GPR54 Signaling in Mouse NO-Synthesizing Neurons Participates in the Hypothalamic Control of Ovulation

Parkash²,

et al. 2012

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“…Primary tanycyte cultures were prepared from 10‐day‐old male Sprague Dawley rat pups as previously described (Bolborea et al, 2015; De Seranno et al, 2004; Prevot et al, 2003). Brains were removed under sterile conditions, placed in ice‐cold DMEM/F‐12 medium containing penicillin/streptomycin and 25 mM HEPES and the median eminence dissected.…”

Section: Methodsmentioning

confidence: 99%

Thyroid hormone activation of retinoic acid synthesis in hypothalamic tanycytes

Stoney

Helfer

Rodrigues

et al. 2015

Glia

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Thyroid hormone (TH) is essential for adult brain function and its actions include several key roles in the hypothalamus. Although TH controls gene expression via specific TH receptors of the nuclear receptor class, surprisingly few genes have been demonstrated to be directly regulated by TH in the hypothalamus, or the adult brain as a whole. This study explored the rapid induction by TH of retinaldehyde dehydrogenase 1 (Raldh1), encoding a retinoic acid (RA)‐synthesizing enzyme, as a gene specifically expressed in hypothalamic tanycytes, cells that mediate a number of actions of TH in the hypothalamus. The resulting increase in RA may then regulate gene expression via the RA receptors, also of the nuclear receptor class. In vivo exposure of the rat to TH led to a significant and rapid increase in hypothalamic Raldh1 within 4 hours. That this may lead to an in vivo increase in RA is suggested by the later induction by TH of the RA‐responsive gene Cyp26b1. To explore the actions of RA in the hypothalamus as a potential mediator of TH control of gene regulation, an ex vivo hypothalamic rat slice culture method was developed in which the Raldh1‐expressing tanycytes were maintained. These slice cultures confirmed that TH did not act on genes regulating energy balance but could induce Raldh1. RA has the potential to upregulate expression of genes involved in growth and appetite, Ghrh and Agrp. This regulation is acutely sensitive to epigenetic changes, as has been shown for TH action in vivo. These results indicate that sequential triggering of two nuclear receptor signalling systems has the capability to mediate some of the functions of TH in the hypothalamus. GLIA 2016;64:425–439

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“…To identify astrocytes, we stained the sections (overnight at 4°C) with monoclonal antibodies to GFAP (1:5000; Sigma) and developed the reaction the next day with Texas Red goat anti-mouse IgG (1:250; Jackson ImmunoResearch). Tanycytes were identified using monoclonal antibodies against vimentin (1:600; Neomarkers, Union City, CA), a cytoskeletal protein used as a marker for these cells (Chauvet et al, 1998;De Seranno et al, 2004). When immunostaining for TGF␣ and TACE, the growth factor was identified using rabbit polyclonal antibodies (1:200; Peprotech), and the reaction was developed to a green color using biotinylated donkey anti-rabbit Ig (1:250; Jackson ImmunoResearch), followed by fluorescein-conjugated streptavidin (1:250; Jackson ImmunoResearch).…”

Section: Methodsmentioning

confidence: 99%

Hypothalamic Tumor Necrosis Factor-α Converting Enzyme Mediates Excitatory Amino Acid-Dependent Neuron-to-Glia Signaling in the Neuroendocrine Brain

Lomniczi¹,

Cornea²,

Costa³

et al. 2006

J. Neurosci.

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Glial erbB1 receptors play a significant role in the hypothalamic control of female puberty. Activation of these receptors by transforming growth factor ␣ (TGF␣) results in production of prostaglandin E 2 , which then stimulates luteinizing hormone releasing hormone (LHRH) neurons to secrete LHRH, the neuropeptide controlling sexual development. Glutamatergic neurons set in motion this glia-toneuron signaling pathway by transactivating erbB1 receptors via coactivation of AMPA receptors (AMPARs) and metabotropic glutamate receptors (mGluRs). Because the metalloproteinase tumor necrosis factor ␣ converting enzyme (TACE) releases TGF␣ from its transmembrane precursor before TGF␣ can bind to erbB1 receptors, we sought to determine whether TACE is required for excitatory amino acids to activate the TGF␣-erbB1 signaling module in hypothalamic astrocytes, and thus facilitate the advent of puberty. Coactivation of astrocytic AMPARs and mGluRs caused extracellular Ca 2ϩ influx, a Ca 2ϩ /protein kinase C-dependent increase in TACE-like activity, and enhanced release of TGF␣. Within the hypothalamus, TACE is most abundantly expressed in astrocytes of the median eminence (ME), and its enzymatic activity increases selectively in this region at the time of the first preovulatory surge of gonadotropins. ME explants respond to stimulation of AMPARs and mGluRs with LHRH release, and this response is prevented by blocking TACE activity. In vivo inhibition of TACE activity targeted to the ME delayed the age at first ovulation, indicating that ME-specific changes in TACE activity are required for the normal timing of puberty. These results suggest that TACE is a component of the neuron-to-glia signaling process used by glutamatergic neurons to control female sexual development.

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Vascular Endothelial Cells Promote Acute Plasticity in Ependymoglial Cells of the Neuroendocrine Brain

Cited by 72 publications

References 57 publications

Kisspeptin-GPR54 Signaling in Mouse NO-Synthesizing Neurons Participates in the Hypothalamic Control of Ovulation

Kisspeptin-GPR54 Signaling in Mouse NO-Synthesizing Neurons Participates in the Hypothalamic Control of Ovulation

Thyroid hormone activation of retinoic acid synthesis in hypothalamic tanycytes

Hypothalamic Tumor Necrosis Factor-α Converting Enzyme Mediates Excitatory Amino Acid-Dependent Neuron-to-Glia Signaling in the Neuroendocrine Brain

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