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293 results on '"Rostène, W."'

12. 3D Distribution of Tyrosine Hydroxylase, Vasopressin and Oxytocin Neurons in the Transparent Postnatal Mouse Brain

Author

Godefroy, D., Dominici, C., Hardin-Pouzet, H., Anouar, Y., Melik-Parsadaniantz, S., Rostène, W., Goazigo, A. Reaux-Le, Institut de la Vision, Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Différenciation et communication neuronale et neuroendocrine (DC2N), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neuroplasticité des comportements de reproduction = Neuroplasticity of Reproductive Behaviors (NPS-11), Neurosciences Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Neuroscience Paris Seine (NPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut de Biologie Paris Seine (IBPS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Pierre et Marie Curie - Paris 6 (UPMC), and HAL-UPMC, Gestionnaire

Subjects
[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, [SDV.NEU.NB] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology
Abstract

International audience; Over the years, advances in immunohistochemistry techniques have been a critical step in detecting and mapping neuromodulatory substances in the central nervous system. The better quality and specificity of primary antibodies, new staining procedures and the spectacular development of imaging technologies have allowed such progress. Very recently, new methods permitting tissue transparency have been successfully used on brain tissues. In this work, we combined whole-mount immunostaining for tyrosine hydroxylase (TH), oxytocin (OXT) and arginine vasopressin (AVP), with iDISCO+ clearing method, light-sheet microscopy and semi automated counting of 3D-labelled neurons to obtain a 3D distribution of these neuronal populations in a 5-day postnatal (P5) mouse brain. Segmentation procedure and 3D reconstruction allowed us to map with high resolution TH staining the various catecholaminergic cell groups and their ascending and descending fiber pathways. We show that TH pathways are present in the whole P5 mouse brain, similar to what was observed in the adult rat brain.

Published
2017

21. Transcriptional regulation of the tyrosine hydroxylase gene by neurotensin in human neuroblastoma CHP212 cells.

Author

UCL - MD/FSIO - Département de physiologie et pharmacologie, UCL - MD/GYPE - Département de gynécologie, d'obstétrique et de pédiatrie, UCL - (SLuc) Service de gastro-entérologie et hépatologie pédiatrique, Najimi, Mustapha, Hermans, Emmanuel, Rostène, W, Forgez, P, UCL - MD/FSIO - Département de physiologie et pharmacologie, UCL - MD/GYPE - Département de gynécologie, d'obstétrique et de pédiatrie, UCL - (SLuc) Service de gastro-entérologie et hépatologie pédiatrique, Najimi, Mustapha, Hermans, Emmanuel, Rostène, W, and Forgez, P

Abstract

The human neuroblastoma cell line CHP212 was found to express functional high affinity neurotensin (NTS-1) receptor subtype. Based on the functional interactions between neurotensin and dopamine transmission, we have used this cell line to investigate the short- and long-term modulation of tyrosine hydroxylase gene expression by the stable neurotensin agonist JMV 449. After exposure of the cells to 1 microM JMV 449 for 5 or 72 h, tyrosine hydroxylase protein and mRNA levels were significantly increased as detected by western blot analysis and quantitative RT-PCR, respectively. Transfection of CHP212 cells with a plasmid containing the luciferase reporter gene under the control of a limited proximal region of the cloned tyrosine hydroxylase promoter, revealed that the effect of JMV 449 results from an increase in the transcriptional activity of the TH gene. These results indicate that modulation of tyrosine hydroxylase gene expression may constitute one of the mechanisms involved in the control of dopamine transmission by neurotensin. Such neurotensin-mediated changes in tyrosine hydroxylase expression may also participate in multiple adaptation processes within the central nervous system to environmental conditions where neurotensin is released such as stress and food intake.

Published
2001

42. Invited speaker — Non-peptide neurotensin antagonists

Author

Gully, D., primary, Boigegrain, R., additional, Poncelet, M., additional, Heaulme, M., additional, Kitabgi, P., additional, Labbé-Jullié, C., additional, Rostène, W., additional, Brouard, A., additional, Maffrand, J.P., additional, and Le Fur, G., additional

Published
1993
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45. Evaluation of the protective effect of oestradiol against toxicity induced by 6-hydroxydopamine and 1-methyl-4-phenylpyridinium ion (MPP[sup +]) towards dopaminergic mesencephalic neurones in primary culture.

Author

Callier, S., Saux, M.L., Lhiaubet, A-M., Paolo, T.D., Rostène, W., and Pelaprat, D.

Subjects
ESTRADIOL, DOPAMINERGIC neurons, TOXINS
Abstract

Recent findings suggest that gonadal steroid hormones are neuroprotective and may provide clinical benefits in delaying the development of Parkinson's disease. In this report we investigated the ability of oestradiol to protect mesencephalic dopaminergic neurones cultured in serum-free or serum-supplemented medium from toxicity induced by 6-hydroxydopamine or 1-methyl-4-phenylpyridinium ion (MPP[sup +]). The efficiency of both toxins and oestradiol was evaluated by tyrosine hydroxylase (TH) immunocytochemistry, [[sup 3]H]dopamine ([[sup 3]H]DA) uptake, length of dopaminergic processes and␣lactate dehydrogenase (LDH) release measurement. In␣cultures grown in serum-supplemented medium, a 2-h pre-treatment with high concentrations (10–100 µm) of 17β-oestradiol or 17α-oestradiol, the stereoisomer with weak oestrogenic activity, protected both dopaminergic and non-dopaminergic neurones from toxicity induced by 6-hydroxydopamine (6-OHDA; 40 or 100 µm) and by the high MPP[sup +] concentrations (50 µm) necessary to obtain significant neuronal death under those culture conditions. At these concentrations, MPP[sup +] was no longer selective for dopaminergic neurones but affected all cells present in the culture. In contrast, the hormonal treatments did not protect against selective degeneration of dopaminergic neurones induced by lower MPP[sup +] concentrations (below 10 µm), related to inhibition of complex I of respiratory chain. In cultures grown in serum-free medium, oestradiol concentrations higher than 1 µm induced neuronal degeneration and no protection against 6-OHDA or MPP[sup +] toxicity was observed at lower concentrations of the steroid. The neuroprotective effects of 17α- or 17β-oestradiol evidenced in this model might be due to the antioxidant properties of these compounds. However, other non-genomic effects of the steroids cannot be excluded. [ABSTRACT FROM AUTHOR]

Published
2002
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50. Dexamethasone Downregulates Chemokine Receptor CXCR4 and Exerts Neuroprotection against Hypoxia/Ischemia-Induced Brain Injury in Neonatal Rats

Author

Felszeghy, K., Banisadr, G., Rostène, W., Nyakas, C., and Haour, F.

Abstract

AbstractObjective: Hypoxia/ischemia (H/I) induces rapid and massive brain damage in neonatal rat brain, resulting in long-term consequences on structural and functional maturation of the central nervous system. Inflammatory mediators contribute to these permanent pathological changes, which are sensitive to corticoid treatments. Since the chemokine receptor CXCR4, specific for the SDF-1α/CXCL12 ligand, regulates both apoptotic and neuroregeneration processes, this receptor was quantified 2 days following H/I in neonatal rat brain in relation with dexamethasone (DEX) treatment. Methods: Seven-day-old male rats were exposed to a 90-min hypoxia following unilateral carotid ligation (H/I) and were sacrificed 48 h later. Glucocorticoid-pretreated animals were injected subcutaneously 5 h prior to hypoxia with 0.5 μg/g DEX. Glial fibrillary acidic protein and cresyl violet staining were used for assessing the extent of brain lesion subdivided into necrotic and penumbra-like areas. The density of CXCR4 receptors was determined by quantitative autoradiography using [125I]SDF-1α as a ligand. Results: The H/I resulted in a massive lesion ipsilateral to the carotid ligation, which was extended to cortical, striatal, hippocampal and thalamic areas, while the contralateral hemisphere remained apparently unaffected. DEX decreased the lesion size by reducing mainly the necrotic area. H/I induced a marked increase in CXCR4 receptor binding in the penumbra-like areas. DEX pretreatment decreased CXCR4 receptor density in the penumbra and attenuated astrocytosis. Furthermore, DEX strongly lowered mortality rate and reduced functional recovery time right after hypoxia. Conclusion: The rapid enhancement in CXCR4 chemokine receptor binding in the affected brain areas suggests that SDF-1α/CXCR4 may play a role in the hypoxia-induced inflammatory reaction in the neonatal brain. Attenuation of CXCR4 expression and astrogliosis could contribute to the neuroprotective effect of DEX pretreatment via influencing the inflammatory cascade induced by H/I in the neonatal brain.Copyright © 2004 S. Karger AG, Basel

Published
2004

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