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9. Ocular inflammation induces trigeminal pain, peripheral and central neuroinflammatory mechanisms

Author

Pierre-Serge Launay, Elodie Reboussin, Hong Liang, Karima Kessal, David Godefroy, William Rostene, Jose-Alain Sahel, Christophe Baudouin, Stéphane Melik Parsadaniantz, and Annabelle Reaux Le Goazigo

Subjects
Benzalkonium chloride, Corneal neurons, Ocular pain, Neuroinflammation, Trigeminal complex, Facial motor nucleus, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Ocular surface diseases are among the most frequent ocular pathologies, with prevalence ranging from 20% of the general population. In addition, ocular pain following corneal injury is frequently observed in clinic. The aim of the study was to characterize the peripheral and central neuroinflammatory process in the trigeminal pathways in response to cornea alteration induced by chronic topical instillations of 0.2% benzalkonium chloride (BAC) in male C57BL/6 J mice. In vitro BAC induced neurotoxicity and increases neuronal (FOS, ATF3) and pro-inflammatory (IL-6) markers in primary mouse trigeminal ganglion culture. BAC-treated mice exhibited 7 days after the treatment reduced aqueous tear production and increased inflammatory cell infiltration in the cornea. Hypertonic saline-evoked eye wipe behavior was enhanced in BAC-treated animals that exhibited increased FOS, ATF3 and Iba1 immunoreactivity in the trigeminal ganglion. Ocular inflammation is associated with a significant increase in IL-6 and TNF-α mRNA expression in the trigeminal ganglion. We reported a strong increase in FOS and Iba1 positive cells in particular in the sensory trigeminal complex at the ipsilateral interpolaris/caudalis (Vi/Vc) transition and Vc/upper cervical cord (Vc/C1) regions. In addition, activated microglial cells were tightly wrapped around activated FOS neurons in both regions and phosphorylated p38 mitogen-activated protein kinase was markedly enhanced specifically in microglial cells during ocular inflammation. Similar data were obtained in the facial motor nucleus. These neuroanatomical data correlated with the increase in mRNA expression of pro-inflammatory (TNF-α, IL-6, CCL2) and neuronal (FOS and ATF3) markers. Interestingly, the suppression of corneal inflammation 10 days following the end of BAC treatment resulted in a marked attenuation of peripheral and central changes observed in pathological conditions.This study provides the first demonstration that corneal inflammation induces activation of neurons and microglial p38 MAPK pathway within sensory trigeminal complex. These results suggest that this altered activity in intracellular signaling caused by ocular inflammation might play a priming role in the central sensitization of ocular related brainstem circuits, which represents a significant factor in ocular pain development.

Published
2016
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12. Association of Sensitive Eyes with Sensitive Skin: A Worldwide Study of 10,743 Subjects

Author

Laurent Misery, Annabelle Reaux-Le Goazigo, Stéphane Morisset, Sophie Seite, Véronique Delvigne, Béatrice Cochener, and Charles Taieb

Subjects
Male, Pharmacology, China, genetic structures, Physiology, Dermatology, General Medicine, Skin Diseases, eye diseases, Sunlight, Humans, Female, France, sense organs, Skin
Abstract

Introduction: Sensitive eyes are commonly reported by patients, but there are very few epidemiological studies on this disorder. The aim of this study was the evaluation of the self-reported frequency of sensitive eyes and the association with sensitive skin. Methods: A survey was performed on a representative sample of the population aged more than 18 years in five different countries (Brazil, China, France, Russia, and the USA). All participants answered a questionnaire on sociodemographic characteristics; skin phototype; eye color; tobacco consumption; exposure to sunlight, air pollution, or having pets; and sleep disorders. The presence of sensitive eyes, eyelids, or skin and their triggering factors were assessed with specific questions. Results: A total of 10,743 individuals (5,285 men and 5,458 women) were included in the study. Among them, 48.2% reported having sensitive skin and 46.0% reported having sensitive eyes. Sensitive eyes were more frequently reported by women (46.5%) than men (39.4%) in all countries, with the exception of China. The presence of sensitive eyes was more frequent if skin was very sensitive. More than half of subjects with sensitive eyes declared that their triggering factors were exposure to sunlight, dust, touch pad screens, or computer screens or dry air. They were more exposed to pollution and tobacco. Their phototype (including eye color) was lighter. Discussion/Conclusion: This large study shows that self-declared sensitive eyes are very frequent and commonly associated with sensitive skin. Triggering factors of sensitive eyes are more specific.

Published
2022
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19. Electrical match between initial segment and somatodendritic compartment for action potential backpropagation in retinal ganglion cells

Author

Goethals, Sarah, Sierksma, Martijn C., Nicol, Xavier, Reaux-Le Goazigo, Annabelle, Brette, Romain, Goethals, Sarah, Sierksma, Martijn C., Nicol, Xavier, Reaux-Le Goazigo, Annabelle, and Brette, Romain

Abstract

The action potential of most vertebrate neurons initiates in the axon initial segment (AIS) and is then transmitted to the soma where it is regenerated by somatodendritic sodium channels. For successful transmission, the AIS must produce a strong axial current, so as to depolarize the soma to the threshold for somatic regeneration. Theoretically, this axial current depends on AIS geometry and Na+ conductance density. We measured the axial current of mouse retinal ganglion cells using whole cell recordings with post hoc AIS labeling. We found that this current is large, implying high Na+ conductance density, and carries a charge that covaries with capacitance so as to depolarize the soma by ∼30 mV. Additionally, we observed that the axial current attenuates strongly with depolarization, consistent with sodium channel inactivation, but temporally broadens so as to preserve the transmitted charge. Thus, the AIS appears to be organized so as to reliably backpropagate the axonal action potential.

Published
2021

22. AOP and IATA applied to ocular surface toxicity

Author

Bonneau, Noémie, Baudouin, Christophe, Reaux-Le Goazigo, Annabelle, Brignole-Baudouin, Françoise, Institut Hospitalo-Universitaire FOReSIGHT, Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier National d'Ophtalmologie des Quinze-Vingts (CHNO)-Sorbonne Université (SU), Institut de la Vision, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Horus Pharma, Hôpital Ambroise Paré [AP-HP], Université de Versailles Saint-Quentin-en-Yvelines - UFR Sciences de la santé Simone Veil (UVSQ Santé), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Centre Hospitalier National d'Ophtalmologie des Quinze-Vingts (CHNO), Université Paris Descartes - Faculté de Pharmacie de Paris (UPD5 Pharmacie), Université Paris Descartes - Paris 5 (UPD5), HAL-SU, Gestionnaire, and Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
Computer science, Animal Testing Alternatives, Toxicology, 03 medical and health sciences, 0302 clinical medicine, Toxic Optic Neuropathy, Adverse Outcome Pathway, Animals, Organisation for Economic Co-Operation and Development, 030304 developmental biology, Alternative methods, 0303 health sciences, Ocular Surface, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, Biologic response, General Medicine, In Silico, 3D Multicellular, 3. Good health, Ocular toxicity, Risk analysis (engineering), 030221 ophthalmology & optometry, Draize test, Rabbits, OECD guidelines, Draize Eye Test, Ocular surface, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Until now, the Draize test on rabbits has been the only test performed to anticipate ocular toxicity of pharmaceutical compounds, mainly irritation. The OECD is urging the scientific community to develop and validate alternative methods to reduce the need for animal testing. Since the models and tests used cannot reflect the entire biologic response, it is necessary to combine them into integrated approaches to testing and assessment (IATA) to obtain robust data. IATAs, along with adverse outcome pathways (AOP) that encompass molecular cascades and key events, require the best combinations of tests. This commentary manuscript describes these OECD tools and proposes original approaches for ocular surface AOP and an IATA for toxicity-induced dry eye (TIDE).

Published
2021
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23. Apelin

Author

Reaux-Le Goazigo, A., primary, Iturrioz, X., additional, and Llorens-Cortes, C., additional

Published
2009
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25. Effects of corneal injury on ciliary nerve fibre activity and corneal nociception in mice: A behavioural and electrophysiological study

Author

Joubert F, Acosta M, Gallar J, Fakih D, Sahel J, Baudouin C, Bodineau L, Parsadaniantz S, and Reaux-Le Goazigo A

Subjects
genetic structures, sense organs, eye diseases
Abstract

Background Ocular surface diseases are among the most frequent ocular pathologies. Ocular pain following corneal injury is frequently observed in clinic. Corneal sensory innervation is supplied by ciliary nerves derived from ophthalmic division of the trigeminal ganglion. Methods & Results Extracellular activity of the mouse ciliary nerve was first used to investigate the corneal responsiveness to chemical, mechanical and thermal stimulations in order to specifically study the responses of polymodal nociceptors, mechano-nociceptors and cold thermoreceptor in a control cornea. Then, in two models of corneal injury (repeated instillations of 0.02% benzalkonium chloride and corneal scraping), we first measured the corneal sensitivity to chemical (eye-wiping test) and mechanical (von Frey filaments) stimulation. Thereafter, we evaluated whether these corneal injuries modified the spontaneous and chemical stimulation-evoked activity of the ciliary nerve. Both models of injury induced a significant corneal chemical hypersensitivity correlated with an increase of the spontaneous activity of the ciliary nerve and a faster response of the ciliary nerve after a chemical stimulation. Conclusions Overall, this study provides new insights into the functional aspects of corneal nerve fibre activity in mice after corneal injury. The increase in ciliary nerve activity may thus contribute to the development of ocular pain after corneal damage. Significance: This study highlights the parallel increase in ciliary nerve activity and corneal sensitivity after corneal injury in mice. The strategy of combining ex vivo electrophysiological recordings of the ciliary nerve in mice and corneal sensitivity measurements therefore helps to uncover the functional aspects of corneal pain.

Published
2019

26. Dégénérescences rétinienne et trabéculaire dans le glaucome : pathogenèse et perspectives thérapeutiques

Author

Alexandre Denoyer, Christophe Roubeix, C. Baudouin, A. Reaux-Le Goazigo, Stéphane Mélik-Parsadaniantz, and Anaïs Sapienza

Subjects
Retinal degeneration, Retina, genetic structures, business.industry, Neurodegeneration, Glaucoma, Retinal, medicine.disease, Neuroprotection, eye diseases, Ophthalmology, chemistry.chemical_compound, medicine.anatomical_structure, Retinal ganglion cell, chemistry, medicine, sense organs, Trabecular meshwork, business, Neuroscience
Abstract

Academic and industrial research has brought new insights into the pathogenesis of glaucoma, aiming at identifying and targeting specific mechanisms to improve our current therapeutic strategy. Retinal neurodegeneration is still the main focus, whether in terms of extrinsic factors such as neurotrophin deprivation, glutamate toxicity, vascular deficiency and neuro-inflammation from glial cells, or in terms of retinal ganglion cell intrinsic sensibility to proapoptotic signals. However, glaucoma is not solely a retinal disease but also involves retinal and trabecular meshwork degeneration, extending into and/or even originating from the brain. The present review summarizes our current knowledge of key mechanisms involved in glaucoma degeneration, focusing on the direction of current research towards the future of glaucoma therapy.

Published
2015
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27. La douleur oculaire chronique : mieux la comprendre pour mieux la traiter

Author

Reaux-Le-Goazigo, Annabelle, Labbé, Antoine, Baudouin, Christophe, Melik Parsadaniantz, Stéphane, Institut de la Vision, and 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)

Subjects
[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

International audience; Dry eye symptoms are one of the leading complaints in ophthalmology. They include visual disturbance, various types of symptoms and variable intensity of pain and discomfort that may become chronic or permanent and thus affect significantly the quality of life of patients. Nevertheless, the pathophysiological mechanisms of ocular surface pain remain largely unknown. A better clinical characterization of chronic ocular pain and an understanding of the molecular and cellular mechanisms involved are crucial issues for developing effective management and therapeutic strategy to alleviate ocular pain. In this review, we first describe the nociceptive corneal nerve pathways and the classification of corneal sensitive receptors neurons. The second part of this review gives an update of the preclinical and clinical data related to the inflammatory processes linked to inflammatory ocular pain. The last section describes the various diagnostic tools used in the clinic to evaluate corneal sensitivity and corneal inflammation.; La sècheresse oculaire est un des premiers motifs de consultation en ophtalmologie. Sa prévalence varie de 5 à 35 % chez des sujets âgés de plus de 50 ans. Cette pathologie du segment antérieur de l’œil est caractérisée par des sensations de douleur variables dans leurs intensités, allant du simple inconfort à une douleur oculaire prononcée. Les douleurs oculaires sont très invalidantes et très difficiles à traiter, et leurs mécanismes physiopathologiques demeurent mal connus de nos jours. Ce constat impose un approfondissement de nos connaissances fondamentales sur l’anatomie du système nociceptif cornéen et sur les mécanismes cellulaires impliqués dans l’initiation et la chronicisation de la douleur oculaire. Cette revue présente, dans une première partie, l’anatomie de l’innervation cornéenne et les différentes classes de récepteurs sensitifs cornéens. La seconde partie fait un état des lieux des données précliniques et cliniques portant sur les mécanismes inflammatoires mis en jeu dans cette pathologie. Enfin la dernière partie de cette revue décrit les différents dispositifs actuellement utilisés pour évaluer la douleur et l’inflammation oculaire en clinique humaine.

Published
2017
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31. Three-dimensional distribution of tyrosine hydroxylase, vasopressin and oxytocin neurones in the transparent postnatal mouse brain

Author

H. Hardin-Pouzet, A. Reaux-Le Goazigo, William Rostène, Stéphane Mélik-Parsadaniantz, David Godefroy, Youssef Anouar, and C. Dominici

Subjects
Male, 0301 basic medicine, medicine.medical_specialty, Vasopressin, Tyrosine 3-Monooxygenase, Vasopressins, Endocrinology, Diabetes and Metabolism, Central nervous system, Neuropeptide, Biology, Oxytocin, 03 medical and health sciences, Cellular and Molecular Neuroscience, chemistry.chemical_compound, Imaging, Three-Dimensional, 0302 clinical medicine, Endocrinology, Internal medicine, medicine, Animals, Neurotransmitter, Neurons, Tyrosine hydroxylase, Endocrine and Autonomic Systems, Brain, Immunohistochemistry, Mice, Inbred C57BL, 030104 developmental biology, medicine.anatomical_structure, nervous system, chemistry, Female, Catecholaminergic cell groups, hormones, hormone substitutes, and hormone antagonists, 030217 neurology & neurosurgery, Immunostaining, medicine.drug
Abstract

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 the present study, we combined whole-mount immunostaining for tyrosine hydroxylase (TH), oxytocin (OXT) and arginine vasopressin (AVP), with the iDISCO+ clearing method, light-sheet microscopy and semi-automated counting of three-dimensionally-labelled neurones to obtain a (3D) distribution of these neuronal populations in a 5-day postnatal (P5) mouse brain. Segmentation procedure and 3D reconstruction allowed us, with high resolution, to map TH staining of the various catecholaminergic cell groups and their ascending and descending fibre pathways. We show that TH pathways are present in the whole P5 mouse brain, similar to that observed in the adult rat brain. We also provide new information on the postnatal distribution of OXT and AVP immunoreactive cells in the mouse hypothalamus, and show that, compared to AVP neurones, OXT neurones in the supraoptic (SON) and paraventricular (PVN) nuclei are not yet mature in the early postnatal period. 3D semi-automatic quantitative analysis of the PVN reveals that OXT cell bodies are more numerous than AVP neurones, although their immunoreactive soma have a volume half smaller. More AVP nerve fibres compared to OXT were observed in the PVN and the retrochiasmatic area. In conclusion, the results of the present study demonstrate the utility and the potency of imaging large brain tissues with clearing procedures coupled to novel 3D imaging technologies to study, localise and quantify neurotransmitter substances involved in brain and neuroendocrine functions.

Published
2017
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33. Bilateral neuroinflammatory processes in visual pathways induced by unilateral ocular hypertension in the rat

Author

Sapienza, Anaïs, primary, Raveu, Anne-Laure, additional, Reboussin, Elodie, additional, Roubeix, Christophe, additional, Boucher, Céline, additional, Dégardin, Julie, additional, Godefroy, David, additional, Rostène, William, additional, Reaux-Le Goazigo, Annabelle, additional, Baudouin, Christophe, additional, and Melik Parsadaniantz, Stéphane, additional

Published
2016
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34. Implication of the chemokine CCL2 in trigeminal nociception and traumatic neuropathic orofacial pain

Author

C, Dauvergne, J, Molet, A, Reaux-Le Goazigo, A, Mauborgne, S, Mélik-Parsadaniantz, Y, Boucher, and M, Pohl

Subjects
Male, Nociception, Rats, Sprague-Dawley, Pyrrolidines, Trigeminal Ganglion, Facial Pain, Hyperalgesia, Receptors, CCR2, Animals, Neuralgia, Chemokine CCL2, Rats, Signal Transduction
Abstract

Chemokine (C-C motif) ligand 2 (CCL2) participates in different mechanisms contributing to the spinal cord inflammation and pain development after sciatic nerve injury. Recent data also support its role in orofacial thermal hypersensitivity, although its implication in different phases of trigeminal pain emergence is unclear. We assessed the importance of CCL2 signalling in biochemical and behavioural alterations during the early and late stages following chronic constriction injury of infraorbital nerve (ION-CCI), a model of peripheral traumatic trigeminal pain.After evaluating the consequences of CCL2 intracisternal injection in naïve rats, we determined the expression changes for CCL2, inflammatory and glia activation markers in the somatosensory trigeminal complex (STC) and trigeminal ganglia (TG) after ION-CCI. The role of CCL2 signalling was assessed using pre-emptive or 'curative' intracisternal treatment with specific CCL2 receptor antagonist - INCB3344.Exogenous CCL2 evoked spontaneous behaviour reminiscent of orofacial pain and marked mechanical hypersensitivity, associated with increased expression of proinflammatory cytokines and glial markers in STC and TG. CCL2-evoked changes were prevented by the co-administration of INCB3344. Two weeks after ION-CCI, mRNA for CCL2, glial and inflammatory markers were up-regulated, and CCL2-immunoreactivity accumulated in central and ganglionic tissues. At this time, repeated intracisternal administration of INCB3344 did not attenuate the ION-CCI-associated behavioural nor biochemical changes. By contrast, pre-emptive INCB3344 treatment delayed the emergence of trigeminal mechanical allodynia and associated biochemical alterations.Our data suggest that CCL2 is involved principally in the early events accompanying the ION lesion rather than in long-term alterations and the maintenance of trigeminal mechanical hypersensitivity.

Published
2013

35. Abstract # 1835 Corneal injury induces trigeminal pain, peripheral and central neuroinflammatory process

Author

Pierre-Serge Launay, Elodie Reboussin, William Rostène, Karima Kessal, David Godefroy, Christophe Baudouin, José-Alain Sahel, A. Reaux Le Goazigo, S. Melik Parsadaniantz, and Hong Liang

Subjects
ATF3, education.field_of_study, Pathology, medicine.medical_specialty, genetic structures, Endocrine and Autonomic Systems, business.industry, Immunology, Population, Inflammation, CCL2, Corneal inflammation, eye diseases, Behavioral Neuroscience, Trigeminal ganglion, medicine.anatomical_structure, Cornea, medicine, Tumor necrosis factor alpha, sense organs, medicine.symptom, education, business
Abstract

Ocular surface diseases are among the most frequent ocular pathologies, with prevalence ranging from 20% of the general population. Ocular pain following corneal injury is frequently observed in clinic. Here we characterized the peripheral and central neuroinflammatory process in the trigeminal pathways in response to ocular pain. We used topical instillations of 0.2% benzalkonium chloride (BAC) in mice for 7 days. BAC-treated animals developed severe dry eye (reduced tear production and inflammation in the cornea). Hypertonic saline-evoked eye wipe behavior was enhanced in BAC-treated animals. We reported an increased ATF3, FOS and Iba1 immunoreactivity and higher IL-6 and TNF- α mRNA levels in the trigeminal ganglion. Interestingly, the sensory trigeminal complex at the ipsilateral interpolaris/caudalis (Vi/Vc) transition and Vc/upper cervical cord (Vc/C1) regions exhibited higher FOS and Iba1 positive cells in BAC animals. Activated microglial cells were tightly wrapped around activated FOS neurons in both regions. Furthermore, phosphorylated p38 MAPK was markedly enhanced in microglial cells during ocular inflammation. These neuroanatomical data correlated with the increase in mRNA expression of pro-inflammatory (TNF- α , IL-6, CCL2) and neuronal (FOS and ATF3) markers. This work provides the demonstration that corneal inflammation provokes central neuroinflammatory process. Thus, altered activity in intracellular signaling caused by ocular inflammation might play a priming role in the central sensitization of ocular related brainstem circuits, which represents a significant factor in ocular pain development.

Published
2016
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36. Cellular and subcellular localization of CXCL12 and CXCR4 in rat nociceptive structures: physiological relevance

Author

Annabelle, Reaux-Le Goazigo, Cyril, Rivat, Patrick, Kitabgi, Michel, Pohl, and Stéphane, Melik Parsadaniantz

Subjects
Male, Rats, Sprague-Dawley, Receptors, CXCR4, Spinal Cord, Presynaptic Terminals, Animals, Nociceptors, Sciatic Nerve, Chemokine CXCL12, Rats
Abstract

Initial studies implicated the chemokine CXC motif ligand 12 (CXCL12) and its cognate CXC motif receptor 4 (CXCR4) in pain modulation. However, there has been no description of the distribution, transport and axonal sorting of CXCL12 and CXCR4 in rat nociceptive structures, and their direct participation in nociception modulation has not been demonstrated. Here, we report that acute intrathecal administration of CXCL12 induced mechanical hypersensitivity in naive rats. This effect was prevented by a CXCR4-neutralizing antibody. To determine the morphological basis of this behavioural response, we used light and electron microscopic immunohistochemistry to map CXCL12- and CXCR4-immunoreactive elements in dorsal root ganglia, lumbar spinal cord, sciatic nerve and skin. Light microscopy analysis revealed CXCL12 and CXCR4 immunoreactivity in calcitonin gene related peptide-containing peptidergic primary sensory neurons, which were both conveyed to central and peripheral sensory nerve terminals. Electron microscopy clearly demonstrated CXCL12 and CXCR4 immunoreactivity in primary sensory nerve terminals in the dorsal horn; both were sorted into small clear vesicles and large dense-core vesicles. This suggests that CXCL12 and CXCR4 are trafficked from nerve cell bodies to the dorsal horn. Double immunogold labelling for CXCL12 and calcitonin gene related peptide revealed partial vesicular colocalization in axonal terminals. We report, for the first time, that CXCR4 receptors are mainly located on the neuronal plasma membrane, where they are present at pre-synaptic and post-synaptic sites of central terminals. Receptor inactivation experiments, behavioural studies and morphological analyses provide strong evidence that the CXCL12/CXCR4 system is involved in modulation of nociceptive signalling.

Published
2012

37. Neurochemokines: a menage a trois providing new insights on the functions of chemokines in the central nervous system

Author

William Rostène, Marc-André Dansereau, David Godefroy, Juliette van Steenwinckel, Annabelle Reaux-Le Goazigo, stephane melik parsadaniantz, Emmanuelle Apartis, Stéphane Hunot, Nicolas Beaudet, Philippe Sarret, Institut de la Vision, Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Department of Physiology and Biophysics, Université de Sherbrooke (UdeS), 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), Institut National de la Santé et de la Recherche Médicale (INSERM), Service d'explorations fonctionnelles [Saint-Antoine], CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Université Pierre et Marie Curie - Paris 6 (UPMC), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), 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)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Central Nervous System, Neurotransmitter Agents, Animals, Humans, [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC], Chemokines, Nervous System Diseases, Models, Biological, ComputingMilieux_MISCELLANEOUS
Abstract

Recent observations suggest that besides their role in the immune system, chemokines have important functions in the brain. There is a great line of evidence to suggest that chemokines are a unique class of neurotransmitters/neuromodulators, which regulate many biological aspects as diverse as neurodevelopment, neuroinflammation and synaptic transmission. In physiopathological conditions, many chemokines are synthesized in activated astrocytes and microglial cells, suggesting their involvement in brain defense mechanisms. However, when evoking chemokine functions in the nervous system, it is important to make a distinction between resting conditions and various pathological states including inflammatory diseases, autoimmune or neurodegenerative disorders in which chemokine functions have been extensively studied. We illustrate here the emergent concept of the neuromodulatory/neurotransmitter activities of neurochemokines and their potential role as a regulatory alarm system and as a group of messenger molecules for the crosstalk between neurons and cells from their surrounding microenvironment. In this deliberately challenging review, we provide novel hypotheses on the role of these subtle messenger molecules in brain functions leading to the evidence that previous dogmas concerning chemokines should be reconsidered.

Published
2011

38. The RFamide neuropeptide 26RFa and its role in the control of neuroendocrine functions

Author

Chartrel, C, Alvear-Perez, P, Iturrioz, X., Reaux-Le Goazigo, A., Audinot, V., Chomarat, C, Coge, C, Nosjean, O., Rodriguez, M., Galizzi, J., Goazigo, R., Chomarat, P., Coge, F., Chartrel, Nicolas, Alonzeau, Jessy, Alexandre, David, Jeandel, Jean, Alvear-Perez, Rodrigo, Leprince, Jérôme, Boutin, Jean, Vaudry, Hubert, Anouar, Youssef, Llorens-Cortes, Catherine, Jeandel, Lydie, Institut de la Vision, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique et Physiologie Intégratives de l'Arbre Fruitier et Forestier (PIAF), Institut National de la Recherche Agronomique (INRA)-Université Blaise Pascal - Clermont-Ferrand 2 (UBP), 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), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), 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)-CHU Pitié-Salpêtrière [APHP], Neuropeptides centraux et régulations hydrique et cardiovasculaire, Université Pierre et Marie Curie - Paris 6 (UPMC)-Collège de France (CdF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Neuroendocrinologie cellulaire et moléculaire, Institut de Recherches Servier, Centre de Recherches de Croissy, Centre interdisciplinaire de recherche en biologie (CIRB), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Collège de France (CdF)-PSL Research University (PSL), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU), Collège de France (CdF)-Institut National de la Santé et de la Recherche Médicale (INSERM)-PSL Research University (PSL)-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)-CHU Pitié-Salpêtrière [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre interdisciplinaire de recherche en biologie (CIRB), Labex MemoLife, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Labex MemoLife, Université Paris sciences et lettres (PSL)-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), Université Paris sciences et lettres (PSL)-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)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), 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)-CHU Pitié-Salpêtrière [AP-HP], Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre interdisciplinaire de recherche en biologie (CIRB), École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Ecole Superieure de Physique et de Chimie Industrielles de la Ville de Paris (ESPCI Paris), Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-École normale supérieure - Paris (ENS Paris), Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Labex MemoLife, and Université Paris sciences et lettres (PSL)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, MESH: Amino Acid Sequence, MESH: Receptors, G-Protein-Coupled, [CHIM.THER]Chemical Sciences/Medicinal Chemistry, MESH: Neuropeptides, Receptors, G-Protein-Coupled, 0302 clinical medicine, MESH: Pituitary Gland, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], MESH: Ligands, MESH: Animals, Tissue Distribution, Receptor, Peptide sequence, MESH: Vertebrates, MESH: Cyclic AMP, 0303 health sciences, Vertebrate, Cell biology, Hypothalamus, Vertebrates, medicine.medical_specialty, MESH: Ghrelin, Neuropeptide, Biology, Models, Biological, 03 medical and health sciences, Neuroendocrine Cells, biology.animal, Internal medicine, medicine, MESH: Neuroendocrine Cells, MESH: Protein Binding, Animals, Humans, Amino Acid Sequence, MESH: Tissue Distribution, Gene, 030304 developmental biology, G protein-coupled receptor, MESH: Humans, MESH: Molecular Sequence Data, Endocrine and Autonomic Systems, MESH: Transfection, Neuropeptides, QRFP, MESH: Models, Biological, Endocrinology, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, MESH: Peptide Hormones, 030217 neurology & neurosurgery
Abstract

International audience; Identification of novel neuropeptides and their cognate G protein-coupled receptors is essential for a better understanding of neuroendocrine regulations. The RFamide peptides represent a family of regulatory peptides that all possess the Arg-Phe-NH2 motif at their C-terminus. In mammals, seven RFamide peptides encoded by five distinct genes have been characterized. The present review focuses on 26RFa (or QRFP) which is the latest member identified in this family. 26RFa is present in all vertebrate phyla and its C-terminal domain (KGGFXFRF-NH2), which is responsible for its biological activity, has been fully conserved during evolution. 26RFa is the cognate ligand of the orphan G protein-coupled receptor GPR103 that is also present from fish to human. In all vertebrate species studied so far, 26RFa-expressing neurons show a discrete localization in the hypothalamus, suggesting important neuroendocrine activities for this RFamide peptide. Indeed, 26RFa plays a crucial role in the control of feeding behavior in mammals, birds and fish. In addition, 26RFa up-regulates the gonadotropic axis in mammals and fish. Finally, evidence that the 26RFa/GPR103 system regulates steroidogenesis, bone formation, nociceptive transmission and arterial blood pressure has also been reported. Thus, 26RFa appears to act as a key neuropeptide in vertebrates controlling vital neuroendocrine functions. The pathophysiological implication of the 26RFa/GPR103 system in human is totally unknown and some fields of investigation are proposed.

Published
2010
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40. Acute food deprivation reduces expression of diazepam-binding inhibitor, the precursor of the anorexigenic octadecaneuropeptide ODN, in mouse glial cells

Author

Schouft, Marie-Thérèse, Fontaine, Marc, Scalbert, Elisabeth, Malagon, Maria, Gandolfo, Pierrick, Desrues, Laurence, Cellier, Eric, Decker, Annick, Clerens, Stefan, Vandesande, Frans, Do-Rego, C., Beauvillain, C., Baroncini, Marc, Balment, Richard, Dujardin, Cynthia, Tollemer, Helene, BRUZZONE, FEDERICA, Tollemer, Hélène, Do-Régo, Jean, Simonnet, Guy, VALLARINO, MAURO, Beauvillain, Jean, Costentin, Jean, Do-Régo, Jean-Claude, Beauvillain, Jean-Claude, Chartrel, C, Alvear-Perez, P, Iturrioz, X., Reaux-Le Goazigo, A., Audinot, V., Chomarat, C, Coge, C, Nosjean, O., Rodriguez, M., Galizzi, J., Goazigo, R., Chomarat, P., Coge, F., Chartrel, Nicolas, Alonzeau, Jessy, Alexandre, David, Jeandel, Jean, Alvear-Perez, Rodrigo, Boutin, Jean, Anouar, Youssef, Llorens-Cortes, Catherine, Jeandel, Lydie, Carlier, Ludovic, Ségalas-Milazzo, Isabelle, Guilhaudis, Laure, Oulyadi, Hassan, Davoust, Daniel, Dubessy, Christophe, Scalbert, Elizabeth, Pfeiffer, Bruno, Renard, Pierre, Lihrmann, Isabelle, Pacaud, Pierre, Chevrier, Lucie, De Brevern, Alexandre, Hernandez, Eva, Guedj, Anne Marie, de Roux, Nicolas, Cholez, V, Debuysscher, V, Bourgeais, B, Boudot, B, Tron, F., Brassart, B., Regnier, A., Bissac, E, Pecnard, E, Gouilleux, F., Lassoued, K, Gouilleux-Gruart, V, Cholez, E, Bourgeais, J, Boudot, C., Gouilleux, V, Chuquet, Julien, Lecrux, Clotilde, Chatenet, David, Chazalviel, Laurent, Roussel, Simon, MacKenzie, Eric, Touzani, Omar, Tonon, M.C, Li, S., Leprince, J�r�me, Tonon, M.C., Compère, M, Lanfray, D, Castel, Hélène, Morin, M., Leprince, Jérôme, Dureuil, B, Vaudry, Hubert, Pelletier, G., Tonon, Marie-Christine, Compère, V., Morin, F., Dureuil, D, Vaudry, V, inconnu, Inconnu, Neuroendocrinologie cellulaire et moléculaire, Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Différenciation et communication neuronale et neuroendocrine (DC2N), Chercheur indépendant, Laboratoire de l'intégration, du matériau au système (IMS), Centre National de la Recherche Scientifique (CNRS)-Institut Polytechnique de Bordeaux-Université Sciences et Technologies - Bordeaux 1, University of Córdoba [Córdoba], Institut de médecine moléculaire de Rangueil (I2MR), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer (JPArc - U837 Inserm), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université Lille 2 - Faculté de Médecine, UMR 5287, Homéostasie-Allostasie-Pathologie-Réhabilitation, Centre National de la Recherche Scientifique (CNRS), Neuropsycho-pharmacologie expérimentale, Centre National de la Recherche Scientifique (CNRS)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU), Institut de la Vision, Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut de biologie et chimie des protéines [Lyon] (IBCP), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physique et Physiologie Intégratives de l'Arbre Fruitier et Forestier (PIAF), Institut National de la Recherche Agronomique (INRA)-Université Blaise Pascal - Clermont-Ferrand 2 (UBP), Institut du Cerveau et de la Moëlle Epinière = Brain and Spine Institute (ICM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pitié-Salpêtrière [APHP]-Centre National de la Recherche Scientifique (CNRS), Neuropeptides centraux et régulations hydrique et cardiovasculaire, Université Pierre et Marie Curie - Paris 6 (UPMC)-Collège de France (CdF)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Recherches Servier, Centre de Recherches de Croissy, ESPE de l'Académie d'Amiens, Chimie Organique et Bioorganique : Réactivité et Analyse (COBRA), Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie Organique Fine (IRCOF), Normandie Université (NU)-Normandie Université (NU)-Institut national des sciences appliquées Rouen Normandie (INSA Rouen Normandie), Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS), Equipe de Chimie Organique et Biologie Structurale (ECOBS), Institut national des sciences appliquées Rouen Normandie (INSA Rouen Normandie), Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Normandie Université (NU)-Institut National des Sciences Appliquées (INSA), Université Henri Poincaré - Nancy 1 (UHP), Institut de recherches Servier (INSTITUT DE RECHERCHES SERVIER), INSTITUT SERVIER, Les Laboratoires SERVIER, Institut de Recherche Servier, Institut du thorax, Université de Nantes (UN)-IFR26-Institut National de la Santé et de la Recherche Médicale (INSERM), Physiopathologie et neuroprotection des atteintes du cerveau en développement, Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Bioinformatique génomique et moléculaire ((U 726)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Diderot - Paris 7 (UPD7), Service des Maladies Métaboliques et Endocriniennes, Hôpital Universitaire Carémeau [Nîmes], Neuroprotection du Cerveau en Développement / Promoting Research Oriented Towards Early Cns Therapies (PROTECT), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Fédératif de Recherches Multidisciplinaires sur les Peptides (IFRMP 23), Institut National de la Santé et de la Recherche Médicale (INSERM)-CRLCC Henri Becquerel-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Université Le Havre Normandie (ULH), Normandie Université (NU)-CHU Rouen, Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS), Matrice extracellulaire et dynamique cellulaire - UMR 7369 (MEDyC), SFR CAP Santé (Champagne-Ardenne Picardie Santé), Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Centre National de la Recherche Scientifique (CNRS), STMicroelectronics, Génétique, immunothérapie, chimie et cancer (GICC), UMR 6239 CNRS [2008-2011] (GICC UMR 6239 CNRS), Université de Tours-Centre National de la Recherche Scientifique (CNRS), Matrice extracellulaire et régulations cellulaires (MERC), Université de Reims Champagne-Ardenne (URCA)-Centre National de la Recherche Scientifique (CNRS), Institut Armand Frappier (INRS-IAF), Réseau International des Instituts Pasteur (RIIP)-Institut National de la Recherche Scientifique [Québec] (INRS), Neurodégénérescence : modèles et stratégies thérapeutiques (NMST), Centre National de la Recherche Scientifique (CNRS)-Université de Caen Normandie (UNICAEN), Aix-Marseille Université - Faculté de pharmacie (AMU PHARM), Aix Marseille Université (AMU), IRCELYON-Ingéniérie, du matériau au réacteur (ING), Institut de recherches sur la catalyse et l'environnement de Lyon (IRCELYON), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Télécom SudParis (TSP), Université Sciences et Technologies - Bordeaux 1-Institut Polytechnique de Bordeaux-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Lille 2 - Faculté de Médecine -Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Rouen Normandie (UNIROUEN), 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)-CHU Pitié-Salpêtrière [APHP], CHU Rouen, Normandie Université (NU)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-CRLCC Henri Becquerel-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Recherche Scientifique [Québec] (INRS)-Réseau International des Instituts Pasteur (RIIP), Normandie Université (NU)-Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Sorbonne Université (SU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Pierre et Marie Curie - Paris 6 (UPMC)-Centre interdisciplinaire de recherche en biologie (CIRB), Collège de France (CdF)-Institut National de la Santé et de la Recherche Médicale (INSERM)-PSL Research University (PSL)-Centre National de la Recherche Scientifique (CNRS)-Collège de France (CdF)-Institut National de la Santé et de la Recherche Médicale (INSERM)-PSL Research University (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Chimie Organique Fine (IRCOF), Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Centre National de la Recherche Scientifique (CNRS)-Institut Normand de Chimie Moléculaire Médicinale et Macromoléculaire (INC3M), Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Université Le Havre Normandie (ULH), Normandie Université (NU)-Institut national des sciences appliquées Rouen Normandie (INSA Rouen Normandie), Normandie Université (NU)-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-École Nationale Supérieure d'Ingénieurs de Caen (ENSICAEN), Normandie Université (NU)-Université de Caen Normandie (UNICAEN), Normandie Université (NU)-Centre National de la Recherche Scientifique (CNRS)-Université Le Havre Normandie (ULH), Normandie Université (NU)-École Nationale Supérieure d'Ingénieurs de Caen (ENSICAEN), Hôpital Universitaire Carémeau [Nîmes] (CHU Nîmes), Centre Hospitalier Universitaire de Nîmes (CHU Nîmes)-Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Université de Reims Champagne-Ardenne (URCA)-SFR CAP Santé (Champagne-Ardenne Picardie Santé), and Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Université de Reims Champagne-Ardenne (URCA)-Université de Picardie Jules Verne (UPJV)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Leptin, Male, Transcription, Genetic, MESH: Sequence Homology, Amino Acid, [SDV.NEU.NB]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]/Neurobiology, MESH: Receptors, G-Protein-Coupled, [CHIM.THER]Chemical Sciences/Medicinal Chemistry, MESH: Neuropeptides, Energy homeostasis, MESH: Down-Regulation, MESH: Ependyma, Mice, 0302 clinical medicine, Endocrinology, Lateral Ventricles, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], Insulin, MESH: Animals, MESH: Proline-Rich Protein Domains, MESH: Peptide Fragments, MESH: Lateral Ventricles, Diazepam Binding Inhibitor, 2. Zero hunger, 0303 health sciences, MESH: Ranidae, MESH: Receptors, Kisspeptin-1, Fasting, medicine.anatomical_structure, Hypothalamus, Neuroglia, MESH: Neuroglia, Ependyma, Diazepam binding inhibitor, Injections, Intraperitoneal, MESH: Injections, Intraperitoneal, Protein Binding, MESH: Protein Transport, medicine.medical_specialty, MESH: Rats, Central nervous system, Down-Regulation, Neuropeptide, MESH: Fasting, MESH: Insulin, Biology, 03 medical and health sciences, Internal medicine, medicine, Animals, MESH: Protein Binding, Molecular Biology, MESH: Mice, Third Ventricle, MESH: RNA, Messenger, 030304 developmental biology, MESH: Transcription, Genetic, Neuropeptides, MESH: Time Factors, MESH: Rats, Wistar, MESH: Leptin, MESH: Hypothalamus, Peptide Fragments, MESH: Male, [SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/Pharmacology, MESH: Diazepam Binding Inhibitor, 030217 neurology & neurosurgery, MESH: Third Ventricle
Abstract

In the central nervous system of mammals, the gene encoding diazepam-binding inhibitor (DBI) is exclusively expressed in glial cells. Previous studies have shown that central administration of a DBI processing product, the octadecaneuropeptide ODN, causes a marked inhibition of food consumption in rodents. Paradoxically, however, the effect of food restriction on DBI gene expression has never been investigated. Here, we show that in mice, acute fasting dramatically reduces DBI mRNA levels in the hypothalamus and the ependyma bordering the third and lateral ventricles. I.p. injection of insulin, but not of leptin, selectively stimulated DBI expression in the lateral ventricle area. These data support the notion that glial cells, through the production of endozepines, may relay peripheral signals to neurons involved in the central regulation of energy homeostasis.

Published
2010
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41. Apelin

Author

A. Reaux-Le Goazigo, X. Iturrioz, and C. Llorens-Cortes

Published
2009
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42. Central Neuropeptide Receptors Involved in Water Balance: Application to Apelin

Author

Annette Hus-Citharel, A. Frugière, Nicolas Chartrel, S. El Messari, Catherine Llorens-Cortes, A. Reaux-Le Goazigo, Claude Kordon, Laurence Bodineau, N. De Mota, Hubert Vaudry, Françoise Moos, Xavier Iturrioz, and Alain Beaudet

Subjects
endocrine system, Vasopressin, Angiotensin receptor, Angiotensin II receptor type 1, nervous system, Chemistry, Neuropeptide, Receptor, hormones, hormone substitutes, and hormone antagonists, Apelin receptor, G protein-coupled receptor, Cell biology, Apelin
Abstract

Because G-protein-coupled receptors (GPCRs) constitute excellent putative therapeutic targets, functional characterization of orphan GPCRs through identification of their endogenous ligands has great potential for drug discovery. In an attempt to identify a receptor specific for angiotensin III, we have cloned, by homology from a rat brain cDNA library, a GPCR that shares 90% amino acid sequence identity with the human orphan APJ (putative receptor protein related to the angiotensin receptor AT1) receptor and 31% with the rat AT1A angiotensin receptor. In 1998, the endogenous ligand for the human orphan APJ receptor, i.e., apelin, was isolated from bovine stomach extracts. Apelin, a bioactive peptide, naturally occurs in the brain and plasma as 13 (pE13F) and 17 amino acid (K17F) fragments of a 77 amino acid precursor. The APJ receptor binds with high affinity K17F and pE13F but not the shorter N-terminal-deleted apelin fragments. This receptor is negatively coupled to adenylate cyclase and internalizes following stimulation with K17F and pE13F. Apelin and its receptor are both widely distributed in the brain and are highly expressed in the supraoptic and paraventricular hypothalamic nuclei. Dual labeling studies demonstrate that, within these two types of nuclei, apelin and its receptor co-localize with vasopressin (AVP) in magnocellular neurons. In lactating rodents, characterized by increases in synthesis and release of AVP, central injection of apelin inhibits the phasic electrical activity of AVP neurons and reduces the secretion of AVP in the bloodstream, resulting in aqueous diuresis. Apelin may thus be considered as a natural inhibitor of the anti-diuretic effect of AVP. Moreover, water deprivation, which increases systemic AVP release, decreases plasma apelin concentrations and induces apelin storage inside magnocellular neurons, thereby avoiding the inhibitory action of apelin on AVP release. Thus apelin and AVP are conversely regulated to optimize systemic AVP release and prevent additional water loss at the kidney level.

Published
2006
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43. OR6-3: Early postnatal nutritional programming of growth involves GHRH neurons axon growth stimulation by leptin & IGF-I

Author

Decourtye, L., primary, Mire, E., additional, Clemessy, M., additional, Heurtier, V., additional, Godefroy, D., additional, Cong, R., additional, Ledent, T., additional, Robinson, I., additional, Reaux-Le Goazigo, A., additional, Mollard, P., additional, Meaney, M., additional, Garel, S., additional, Le Bouc, Y., additional, and Kappeler, L., additional

Published
2014
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44. OR6-3: Early postnatal nutritional programming of growth involves GHRH neurons axon growth stimulation by leptin & IGF-I

Author

L. Kappeler, Maud Clemessy, Erik Mire, Patrice Mollard, R. Cong, Lyvianne Decourtye, Tatiana Ledent, Michael J. Meaney, David Godefroy, Iain C. A. F. Robinson, Y. Le Bouc, A. Reaux-Le Goazigo, Victor Heurtier, and Sonia Garel

Subjects
medicine.medical_specialty, Endocrinology, Endocrinology, Diabetes and Metabolism, Internal medicine, Leptin, medicine, Stimulation, Biology, Axon growth
Published
2014
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50. Apelin and Vasopressin

Author

Iturrioz, Xavier, primary, Reaux‐Le Goazigo, Annabelle, additional, Moos, Françoise, additional, and Llorens‐Cortes, Catherine, additional

Published
2008
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