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Lieu: Neurocentre Magendie Seminar room

Journée ARSEP portes ouvertes 2016

Rencontre avec les chercheurs dans les laboratoires dédiés à la Sclérose en plaques

14h : Accueil et présentation du Neurocentre Magendie (Franck Burglen, secrétaire général)
14h30 : Etude des troubles de la mémoire dans la Sclérose en plaques, approche expérimentale chez l’animal (Pr Thomas Tourdias, PU-PH )
15h : Programme rééducation fonctionnelle (Dr Delphine Larmargue Hamel, orthophoniste réseau AQUISEP)
15h30 : Recherche clinique : Troubles cognitifs, mécanisme et détection de la Sclérose en plaques (Pr Bruno Brochet, PU-PH / Dr Mathilde Deloire, coordinatrice étude clinique CHU)




Pour plus de détails: https://www.arsep.org/fr/188-journees-porte-ouverte.html


Séminaire
29/09/2016 09h00
BONNES PRATIQUES DE LABORATOIRES
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Lieu: Neurocentre Magendie Seminar room

Comment optimiser ma technique de pipetage?
Quelle balance choisir pour réaliser mes pesées?
Comment calibrer mon électrode de pH et comment bien l'entretenir?
Ce sont peut-être des questions que vous vous posez...
Pour répondre à toutes ces questions, en partenariat avec Melter Toledo, une journée scientifique est organisée le 29 septembre 2016 au Neurocentre Magendie sur la thématique des BPL.
Accès libre avec cours théoriques et workshops.



Pour plus de détails: neurocentre-magendie.fr/NCM_Downloads/Programme_BPL_Bordeaux.pdf



Lieu: Neurocentre Magendie Seminar room

from University of Trieste's lab will give a presentation entitled 'An in vitro model to study neuronal atrophy and rescue in neurodevelopmental disorders: the case of Rett Syndrome'

Invitant : Daniel Voisin, Neurocentre Magendie / Professor - PhD, University of Bordeaux / Team : Glia-neuron relations


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/enrico-tongiorgi.html



Lieu: Neurocentre Magendie Seminar room

from Department of Pharmacology and Therapeutics (McGill University, Canada) will give a presentation entitled 'Nuclear G proteins in cardiac transcriptional regulation'

Invitant : Stéphane Oliet, Team leader: Glia-neuron relations (Neurocentre Magendie)


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/terry-hebert.html



Lieu: Neurocentre Magendie Seminar room

from Howard Hugues Medical Institute (Washington) will give a presentation entitled 'Chemogenetic ion channel tools for neurobiology'

Invitant : Guillaume LUCAS (Equipe Abrous), Neurocentre Magendie


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/scott-sternson.html


Séminaire
17/06/2016 11h30
Liset Menendez de la Prida
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Lieu: Neurocentre Magendie Seminar room

from Lab Director, Instituto Cajal, Consejo Superior de Investigaciones Cientificas (Madrid, Spain)'s lab will give a presentation entitled "Activity pattern of hippocampal circuits"


Invitant : Xavier Leinekugel (Neurocentre Magendie)


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/de-la-prida.html


Séminaire
02/06/2016 18h00
Apprentis Chercheurs - Véronique Deroche
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Lieu: Centre de Génomique Fonctionnelle

Le projet Apprentis Chercheurs MAAD (Mécanismes des Addictions à l'Alcool et aux Drogues) permet à des jeunes de plusieurs villes françaises de mener des expériences en laboratoire portant sur les addictions pour mieux saisir les mécanismes en oeuvre.
Les participants bordelais présentent leurs travaux le jeudi 2 juin à la PGF. Cette présentation est suivie d'un débat avec Jean-Michel Delile : « Soigner les addictions : la nécessité d’une approche globale ».


Pour plus de détails: http://www.arbre-des-connaissances-apsr.org/wp-content/uploads/2016/05/Flyer_web_Bordeaux_MAAD2016.pdf



Lieu: Neurocentre Magendie Seminar room

from University of Cambridge will give a presentation entitled 'Mitochondrial superoxide production in ischaemia-reperfusion injury'

Invitant : Giovanni Marsicano, Giovanni Marsicano´s Lab / Neurocentre Magendie

Abstract :

Mitochondrial ROS have long been known to contribute to ischaemia-reperfusion (IR) injury in heart attack and stroke, but methods to stop this ROS production were limited. Over the past few years we have developed a mitochondria-targeted S-nitrosating agent, called MitoSNO, that we showed was effective in preventing ROS formation in IR injury with therapeutic implications. In addition, the protection by this compound suggested that ROS production in IR injury was mainly coming from complex I.
This led us to investigate the mechanism of the ROS production and using a metabolomic approach we found that the ROS production in IR injury came from the accumulation of citric acid cycle substrates during ischaemia that then drove mitochondrial ROS production by reverse electron transport at complex I during reperfusion.
This surprising mechanism led up to develop further new therapeutic approaches.


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/mike-murphy.html



Lieu: CGFB Seminar room

from ICM Paris (team leader / Equipe Inhibition synaptique et auto-modulation des microcircuits du cortex cérébral) will give a presentation entitled 'Long-term Plasticity of Neocortical GABAergic Synapses'

Invitant : Giovanni Marsicano, Neurocentre Magendie


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/alberto-bacci.html



Lieu: Neurocentre Magendie Seminar room

Neurotrophins are essential for the maintenance of neuronal homeostasis and modulation of synaptic plasticity. An impairment in the signaling of different neurotrophins such as Brain-derived Neurotrophic Factor (BDNF), Nerve Growth Factor (NGF) and Transforming-Growth-Factor-ß1 (TGF-ß1) has been demonstrated in Alzheimer’s disease (AD) brain in an early phase of the disease.
ß-amyloid (Aβ) accumulation is an early event in AD pathogenesis which can lead to pro-inflammatory processes even before the onset of cognitive decline (Iulita and Cuello 2014). A strong neurobiological link has been found in AD brain between this early pro-inflammatory process and the deficit of neurotrophic factors such as NGF and TGF-ß1. A dysfunction in the extracellular metabolism of NGF that compromises Pro-NGF maturation and exacerbates its subsequent degradation has been recently proposed as a contributor to cholinergic neuron dysfunction in AD and Down Syndrome (DS), and hence to cognitive decline (Iulita, Caraci & Cuello 2016). However, it is not known whether these CNS alterations are reflected in periphery and finally if a relationship exists between Aβ accumulation, peripheral biomarkers related to inflammation and NGF dysfunction in lymphocytes from DS patients with AD. We are currently examining whether DS lymphocytes from DS individuals can reflect, in the periphery, a deficit of NGF known to occur in DS brain in a preclinical stage of AD (Iulita, Caraci & Cuello 2016).
TGF-β1 is an anti-inflammatory cytokine that exerts neuroprotective effects against Aβ-induced neurodegeneration (Caraci et al. 2008). Recently, we have identified a key role for TGF-ß1 in recognition memory formation demonstrating that this neurotrophic factor is essential for the transition from early to late LTP (Caraci et al. 2015). An impairment of TGF-β1 signaling pathway has been demonstrated to be specific to the AD brain, and particularly to the early phase of the disease. Deficit of TGF-β1 seems also to be a common pathophysiological event both in depression and AD. Depression is a risk factor for the development of AD and the presence of depressive symptoms significantly increases the conversion of Mild Cognitive Impairment (MCI) into AD. Plasma TGF-ß1 levels are reduced in major depressed patients, and, interestingly, different second-generation antidepressant drugs increase circulating TGF-ß1 levels in depressed patients. In addition, it is known that continued long-term antidepressants treatment is associated with a reduction in the rate of AD. Whereas these data identify TGF-β1 signaling as a potential common target for both depression and AD, the potential neuroprotective activity of antidepressant drugs against Aβ-induced neurodegeneration in vitro has been only partially explored.
We have examined the neuroprotective activity of fluoxetine and sertraline both in pure and mixed rat neuronal cultures challenged with synthetic Aß(1-42) oligomers (100nM).We found that fluoxetine and sertraline, at therapeutic concentrations (100nM-1µM), significantly prevented Aβ-induced toxicity in mixed cultures, but not in pure neuronal cultures, via a paracrine mechanism mediated by TGF-ß1. Consistent with a glia-mediated effect, a 24 hr treatment of astrocytes with fluoxetine and sertraline promoted the release of TGF-β1 in the culture media by increasing the conversion of Pro-TGF-ß1 to mature TGF-ß1.
Our data demonstrate that second-generation antidepressants are neuroprotective in vitro against Aß-induced neurodegeneration by rescuing TGF-β1 signaling and also suggest that drugs able to increase the release of active TGF-β1, such as fluoxetine and sertraline, might represent new neuroprotective tools for the treatment of AD.


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2016/filipo-caraci.html