BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Bordeaux Neurocampus - ECPv4.9.10//NONSGML v1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
X-WR-CALNAME:Bordeaux Neurocampus
X-ORIGINAL-URL:https://www.bordeaux-neurocampus.fr/en/
X-WR-CALDESC:Events for Bordeaux Neurocampus
BEGIN:VTIMEZONE
TZID:Europe/Paris
BEGIN:DAYLIGHT
TZOFFSETFROM:+0100
TZOFFSETTO:+0200
TZNAME:CEST
DTSTART:20190331T010000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20191027T010000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20191213T093000
DTEND;TZID=Europe/Paris:20191213T113000
DTSTAMP:20260422T143825
CREATED:20190713T123728Z
LAST-MODIFIED:20191210T135938Z
UID:109721-1576229400-1576236600@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Franck Aby
DESCRIPTION:Lieu : Centre Broca Nouvelle-Aquitaine \n\nLes neurones sérotoninergiques du noyau raphé Magnus dans le contrôle de la transmission nociceptive dans la corne dorsale de la moelle épinière : une étude optogénétique dans la physiopathologie douloureuse \nFranck Aby\nIINS – Team Landry\nDirecteur de thèse : Pascal Fossat \n\nRésumé\nLa douleur est une sensation et une expérience émotionnelle désagréable résultant de stimulations potentiellement nuisibles pour protéger l’intégrité du corps. Un mécanisme endogène impliquant le système PAG-RVM\, module la sensation de douleur en filtrant les entrées nociceptives. Un équilibre entre des influences excitatrices et inhibitrices contrôle la transmission nociceptive et une perturbation de cet équilibre conduit à l’installation de douleurs pathologiques. Dans ce travail\, nous avons utilisé une approche optogénétique pour cibler spécifiquement les neurones 5-HT du noyau du raphé Magnus (RMg) projetant sur la corne dorsale de la moelle épinière. Nous avons montré que ces neurones exerçaient une action analgésique tonique par une diminution de l’excitabilité des neurones de projection de la corne dorsale de la moelle épinière. Cet effet étant indépendant du sexe. Nous avons également observé que les neurones 5-HT sont indirectement liés aux neurones de projection par l’intermédiaire d’interneurones inhibiteurs locaux. Puis\, nous avons montré que les neurones 5-HT du RMg recevaient des projections des neurones à somatostatine (SST) du vlPAG exerçant une facilitation descendante de la transmission nociceptive. Fait intéressant\, nous montrons que dans un modèle de neuropathie périphérique\, l’action inhibitrice des neurones à 5-HT du RMg est transformée en influence excitatrice\, aussi bien chez les mâles que les femelles\, en raison d’un déplacement de l’équilibre du chlore au sein de la moelle épinière. Ces résultats suggèrent que la même voie descendante peut être à la fois excitatrice et inhibitrice dans des conditions pathologiques\, révélant des informations cruciales sur les changements à long terme associés à la douleur chronique. \nMots clés : Douleur\, moelle épinière\, réseaux neuronaux\, 5-HT\, SST\, KCC2\, WDR\, excitabilité\, douleur neuropathique\, sexe\, électrophysiologie in vivo\, optogénétique\, pharmacologie. \nPublications:\n– Windup of Nociceptive Flexion Reflex Depends on Synaptic and Intrinsic Properties of Dorsal Horn Neurons in Adult Rat.\nAby\, F; Bouali-Benazzouz\, R; Landry\, M; Fossat\, P.\nPreprints 2019\, 2019100006 https://doi.org/10.3390/ijms20246146 \n– Inflammatory-induced spinal dorsal horn neurons hyperexcitability is mediated by P2X4 receptors.\nAby F\, Whitestone S\, Landry M\, Ulmann L\, Fossat P.\nPain Rep. 2018 May 23;3(3):e660. doi: 10.1097/PR9.0000000000000660. \n– Calcium signalling through L-type calcium channels: role in pathophysiology of spinal nociceptive transmission.\nRoca-Lapirot O\, Radwani H\, Aby F\, Nagy F\, Landry M\, Fossat P.\nBr J Pharmacol. 2018 Jun;175(12):2362-2374. doi: 10.1111/bph.13747. Epub 2017 Mar 24. Review. \n– Group I metabotropic glutamate receptor plasticity after peripheral inflammation alters nociceptive transmission in the dorsal of the spinal cord in adult rats.\nRadwani H\, Roca-Lapirot O\, Aby F\, Lopez-Gonzalez MJ\, Benazzouz R\, Errami M\, Favereaux A\, Landry M\, Fossat P.\nMol Pain. 2017 Jan-Dec;13:1744806917737934. doi: 10.1177/1744806917737934. \nEn révision\nCausal link between developmental n-3 PUFA deficiency and motivation deficits.\nDucrocq\, F and Walle\, R and Contini\, A and Oummadi\, A and Caraballo\, B and Van der Veldt\, S and Boyer\, M and Aby\, F and Tolentino-Cortez\, T and Helbling\, JC and Martine\, L and Grégoire\, S and Cabaret\, S and Vancassel\, S and Layé\, S and Kang\, JX and Fioramonti\, X and Berdeaux\, O and Barreda-Gómez\, G and Masson\, E and Ferreira\, G and Ma\, D W. L. and Bosch-Bouju\, C and De Smedt-Peyrusse\, V and Trifilieff\, P.\nEn revision pour Cell Metabolism\, DOI: 10.2139/ssrn.3382436 \nJury\n\nMme Agnès Nadjar – Professeur – Université de Bordeaux – NutriNeuro – Présidente\nMme Sophie Pezet – Maître de Conférence – ESPCI Paris – Rapportrice\nMr Pierrick Poisbeau – Professeur – Université de Strasbourg – INCI – Rapporteur\nMme Antri Myriam – Maître de Conférence – Neuro-Dol Clermont-Ferrand – Examinatrice\nMr Cyril Herry – Directeur de Recherche – INSERM – Neurocentre Magendie Bordeaux – Membre invité\n\n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-franck-aby/
CATEGORIES:Thesis
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20191213T140000
DTEND;TZID=Europe/Paris:20191213T160000
DTSTAMP:20260422T143825
CREATED:20190713T124108Z
LAST-MODIFIED:20191115T125615Z
UID:109720-1576245600-1576252800@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Eléonore Bertin
DESCRIPTION:Venue: Centre Broca Nouvelle-Aquitaine \nDefense in french \n\nStudy of the increase of P2X4 ATP-gated receptor surface trafficking using novel transgenic murine models: role in memory processes and amyotrophic lateral sclerosis \n(Étude de l’augmentation du trafic en surface des récepteurs P2X4 de l’ATP à l’aide de nouveaux modèles murins transgéniques : implications dans les processus mnésiques et la sclérose latérale amyotrophique) \n\nEléonore Bertin\nTeam E. Bezard (Physiopathologie des syndromes parkinsoniens)\nIMN \nTheis supervisor: Dr. Eric Boué-Grabot \nAbstract\n\nATP signaling and surface P2X4 ATP-gated receptor channels are upregulated in various neurological disorders including amyotrophic lateral sclerosis (ALS)\, a fatal motoneuron (MN) disease characterized by protein misfolding and aggregation leading to cellular degeneration. P2X4 displays a widespread distribution in the central nervous system (CNS) neurons and glial cells as well as in multiple peripheral cell types throughout the body. A key question regarding the role of purinergic signaling in health and disease is the function of this upregulated surface P2X4 state observed in specific cell types. \nTo elucidate the cell-specific functions of P2X4 in a pathological context\, a conditional transgenic knock-in P2X4 mouse line (floxed P2X4mCherryIN) was created allowing the Cre activity-dependent genetic swapping of the internalization motif of P2X4 by the fluorescent protein mCherry to prevent constitutive endocytosis of P2X4. We describe and characterize two distinct knock-in mouse lines expressing non-internalized P2X4mCherryIN either in excitatory forebrain neurons (CamK2) or in all cells natively expressing P2X4 (CMV). The genetic substitution of wild-type P2X4 by non-internalized P2X4mCherryIN in both knock-in mouse models does not alter the sparse distribution and subcellular localization of P2X4 but leads to a cell-specific increased surface P2X4 expression mimicking the pathological upregulated P2X4 state. We provide evidence that the increase in P2X4 at the surface of excitatory neurons decreases anxiety and impairs memory processing due to alteration of synaptic plasticity in the hippocampal CA1 region. \nTo unravel the implication of P2X4 in ALS pathogenesis\, we generate innovating double transgenic mice called SOD1:P2X4KI and SOD1:P2X4KO using the new knock-in CMV mice model expressing the upregulated P2X4 receptor in all cells that expressed natively the P2X4 receptor (P2X4KI) or a trangenic mice lacking the P2X4 gene (P2X4KO) with most commonly used ALS model carrying the human SOD1-G93A mutation (SOD1). Interestingly\, the ablation of the P2X4 gene as well as the expression of non-internalized P2X4 in SOD1 mice have a significant and positive impact on motor performances and animal survival revealing that P2X4 are active and complex players in ALS progression. In SOD1 mice spinal cord\, the expression of P2X4 is initially restricted to MN and increased in microglia during the symptomatic phase of ALS\, and P2X4 has a dual role on inflammation markers expression during the progression of the disease. In parallel\, P2X4 surface expression significantly increased in peritoneal macrophages of SOD1 mice during ALS progression even from the presymptomatic stages suggesting that P2X4 may represent an early biomarker of ALS. Moreover\, we reveal that the mechanism underlying the surface upregulation of P2X4 receptor in ALS models over the time can be explained by a competitive and progressive alteration of P2X4  constitutive internalization by SOD1 misfolded protein leading to MN death and associated neuroinflammation. \nOverall\, we provide an innovative knock-in P2X4 model to study the functional contributions of upregulated P2X4 receptor in specific cells of the nervous system but also in peripheral tissues throughout the body that will be helpful for study many others pathologies besides ALS. \nKeywords: P2X – ALS – transgenic mice \nPublications\nArticles de recherche : \nBertin \, A. Martinez\, A. Fayoux\, P-O. Fernagut\, G. Le Masson\, S.S. Bertrand and E. Boué-Grabot. P2X4 purinoreceptors as key factor in the pathogenesis of ALS and biomarker (en préparation ). \nBertin \, T. Deluc\, K. S. Pilch\, A. Martinez\, J-T Pougnet\, E. Doudnikoff\, A-E Allain\, P. Bergmann\, Russeau\, E. Toulmé\, E. Bezard\, F. Koch-Nolte\, P. Séguéla\, S. Lévi\, B. Bontempi\, F. Georges\, S. S. Bertrand\, O. Nicole and E. Boué-Grabot. (2019) Increased surface P2X4 receptor expression regulates synaptic plasticity and behavior in P2X4 internalization-defective knock-in mice (en révision). \nBertin \, A. Martinez\, A. Ase\, E. Eiselt\, P. Séguéla\, M-B. Emerit and E. Boué-Grabot. Insulin regulates P2X4 receptor function and promotes its rapid delivery to the cell surface (en préparation) \n  \nChapitre de livre : \nBertin \, A. Martinez\, and E. Boué-Grabot. (2020) P2X Electrophysiology and Surface Trafficking in Xenopus Oocytes. Methods in Molecular Biology\, by Humana Press-Springer. \n  \nJury\n\nPascal BRANCHEREAU – Pr. Université de Bordeaux – Président\nMme Séverine BOILLEE -CR\, INSERM\, Paris – Rapportrice\nRodrigo CUNHA Pr. Université de Coimbra – Rapporteur\nMme Lauriane ULMANN  – MCU\, Université de Montpellier -Examinatrice\nMme Sandrine BERTRAND – DR\, CNRS\, Bordeaux – Invitée\nÉric BOUE-GRABOT – DR\, CNRS\, Bordeaux – Directeur de thèse\n\n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-eleonore-bertin/
CATEGORIES:Thesis
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20191213T140000
DTEND;TZID=Europe/Paris:20191213T160000
DTSTAMP:20260422T143825
CREATED:20191203T184031Z
LAST-MODIFIED:20191204T143357Z
UID:113683-1576245600-1576252800@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Vincent Simon
DESCRIPTION:Venue: Neurocentre Magendie \nCharacterization of different subpopulations of hypothalamic POMC neurons in the regulation of energy balance. \nVincent Simon\nNeurocentre Magendie \nThesis supervisor: Daniela Cota \nAbstract\nIntroduction: Obesity is a chronic multifactorial disease\, characterized by a health-threatening accumulation of body fat and whose prevalence has been increasing worldwide since the 1980s. Obesity is a risk factor for type II diabetes\, cardiovascular disease and various forms of cancer and is now a major public health issue. Unfortunately\, available pharmacological treatments are rare and not very effective. Thus\, the study of the biological mechanisms underlying body weight regulation could lead to the discovery of new therapeutic targets and prove useful in the fight against this modern curse. \nThe brain plays a key role in controlling food intake and metabolism. In particular\, some hypothalamic neurons called POMC neurons are classically described as being responsible for satiety. To date\, most studies on these neurons have focused on their neuropeptide production\, but recent discoveries have uncovered the existence of subpopulations\, characterized by their ability to secrete different neurotransmitters (glutamate\, GABA or both). The functional consequences of this unsuspected heterogeneity are largely unknown to this day. \nObjectives: The general objective of this thesis is to study the specific roles of different sub-populations of POMC neurons\, depending on the neurotransmitter they release: we will then distinguish between POMC-Glut (pure glutamatergic)\, POMC-GABA (pure GABAergic) and POMC-Glut/GABA (mixed) neurons. Three objectives have been defined:\n– To develop a new neuroanatomical technical approach to identify subpopulations of activated POMC neurons on brain slices.\n– To determine the impact of a hypercaloric diet on POMC subpopulations.\n– To determine the role of the POMC Glutamatergic population in energy balance by using a novel genetic model. \nResults: First\, we developed a new technique for the simultaneous detection of mRNAs of GAD65/67\, vglut2 and POMC combined with an immunostaining of the cFos protein (a marker of cellular activity)\, in order to identify the subpopulations of activated POMC neurons under various experimental conditions. Then\, we applied this technique in a context of an acute exposure to a high-calorie diet (HFD\, for “high-fat-diet”). We then discovered that POMC-GABA neurons were the main sub-population to be activated by HFD\, unlike POMC-Glut which were less likely to respond to the diet. Of note this preferential activation of POMC-GABA happens in a context of HFD-driven hyperphagia. Finally\, we created a new genetically modified mouse line that allows the deletion of the vglut2 protein from POMC neurons in an inducible way\, thus preventing the release of glutamate from POMC neurons. After carrying out the necessary controls\, we conducted a metabolic characterization of this mouse line. Inducible POMC-vglut2-KO mice\, in which POMC glutamatergic transmission is suppressed\, have an exaggerated hyperphagic response following a 24-hour fast. In addition\, when placed on a HFD\, these mice eat more and have an increased energy expenditure. \nConclusions: This work led to the development of a new neuroanatomical technique whose versatility is a major asset in the study of neurons controlling energy balance\, but which can also be used in many other projects. Our data suggest that there is a functional dichotomy between POMC-Glut and POMC-GABA neurons\, the former playing mainly the expected role of satietogenic POMC neurons\, while activity of the latter is associated with an increase in HFD consumption. Future studies will be necessary to manipulate these different sub-populations and identify their specific sites of action\, in the hope to further clarify their role in the regulation of energy balance. \nKeywords: FISH\, POMC\, glutamate\, GABA\, hypothalamus\, energy balance \nPublications\n\nSimon V\, Cota\, D. (2017). “MECHANISMS IN ENDOCRINOLOGY: Endocannabinoids and metabolism: past\, present and future.” Eur J Endocrinol 176(6): R309-r324.\n\n\nHaissaguerre M.\, Ferrière A\, Simon V\, Saucisse N\, Dupuy N\, André C\, Clark S\, Guzman-Quevedo O\, Tabarin A\, Cota D. (2018). “mTORC1-dependent increase in oxidative metabolism in POMC neurons regulates food intake and action of leptin.” Mol Metab 12: 98-106.\n\n\nMazier W\, Saucisse N\, Simon V\, Cannich A\, Marsicano G\, Massa F\, Cota D. (2019). “mTORC1 and CB1 receptor signaling regulate excitatory glutamatergic inputs onto the hypothalamic paraventricular nucleus in response to energy availability.” Mol Metab 28: 151-159.\n\nJury\n– Mme Agnès NADJAR\, PU\, UMR INRA 1286 – Laboratoire NutriNeurO\, Université de Bordeaux\, France. Présidente et examinatrice.\n– Mme Carole ROVERE\, DR\, UMR CNRS 7275 – Institut de Pharmacologie Moléculaire et Cellulaire (IPMC)\, Université Côte d’Azur\, Nice\, France. Rapporteure.\n– M. Marc CLARET\, Professeur associé\, chef d’équipe – Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)\, Barcelone\, Espagne. Rapporteur.\n– M. Philippe CIOFI\, CR\, INSERM U1215 – Neurocentre Magendie\, Université de Bordeaux\, France. Examinateur.\n– Mme Daniela COTA\, DR\, INSERM U1215 – Neurocentre Magendie\, Université de Bordeaux\, France. Directrice de thèse et membre invitée.\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-vincent-simon/
CATEGORIES:Thesis
END:VEVENT
END:VCALENDAR