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X-WR-CALNAME:Bordeaux Neurocampus
X-ORIGINAL-URL:https://www.bordeaux-neurocampus.fr/en/
X-WR-CALDESC:Events for Bordeaux Neurocampus
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DTSTART;VALUE=DATE:20221219
DTEND;VALUE=DATE:20230619
DTSTAMP:20260602T022712
CREATED:20221215T174158Z
LAST-MODIFIED:20230214T143012Z
UID:153788-1671408000-1687132799@www.bordeaux-neurocampus.fr
SUMMARY:Exposition: Illusions
DESCRIPTION:Lieu : Cap Siences \n\n\n\nEt si le cerveau était un véritable terrain de jeu… Qu’est-ce qu’une illusion ? Comment et pourquoi sommes-nous trompés ? \n\n\n\n\nSi l’illusion naît de nos sens\, elle s’élabore dans le cerveau. Nous voyons\, entendons\, touchons « avec notre cerveau ». Une perception est rarement uni-sensorielle. Plusieurs sens se combinent pour produire une interprétation du monde qui nous entoure : c’est le rôle du cerveau de produire du sens. Il utilise le passé pour s’adapter au présent et dans de nombreux cas compenser le manque d’informations dont il dispose. \nLe cerveau Il tient compte de ce qu’il “sent”\, mais aussi de ce qu’il sait déjà\, de ce que nous avons vécu\, mémorisé. Ce qui nous rend bien des services au quotidien pour prendre des décisions et réagir rapidement ! Mais aussi sophistiqué soit-il\, cet outil peut cependant être trompé par certaines situations… \nCette exposition\, propose une approche interactive à la découverte de nos sens et de nos perceptions. Les manipulations\, des plus simples aux plus impressionnantes troublent les perceptions dans une expérience déroutante. \n\n\n\n\nLe cerveau devient alors un terrain de jeu : Alors\, prêts pour une nouvelle expérience de la réalité ? \n  \n\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/exposition-illusions/
CATEGORIES:Events for all,not-calendar,Semaine du cerveau 2023
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BEGIN:VEVENT
DTSTART;VALUE=DATE:20230208
DTEND;VALUE=DATE:20230302
DTSTAMP:20260602T022712
CREATED:20230201T153931Z
LAST-MODIFIED:20230301T204511Z
UID:155113-1675814400-1677715199@www.bordeaux-neurocampus.fr
SUMMARY:Exposition : Daniela Cota
DESCRIPTION:Daniela Cota\, directrice de recherche Inserm au Neurocentre Magendie\, exposera ses peintures dans l’atrium du centre Broca\, du mercredi 8 février au mercredi 1er mars (décrochage le 2 mars au matin). \nUn portrait réalisé par l’Inserm Nouvelle-Aquitaine lui a récemment été consacré ; elle y partageait sa passion pour la peinture. \n \n
URL:https://www.bordeaux-neurocampus.fr/en/event/exposition-daniela-cota/
CATEGORIES:Entre nous
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BEGIN:VEVENT
DTSTART;VALUE=DATE:20230210
DTEND;VALUE=DATE:20230211
DTSTAMP:20260602T022712
CREATED:20230125T140704Z
LAST-MODIFIED:20230209T091553Z
UID:155009-1675987200-1676073599@www.bordeaux-neurocampus.fr
SUMMARY:Symposium Sanpsy
DESCRIPTION:Centre Broca Nouvelle-Aquitaine \n\nSymposium interne de l’unité Sanpsy (UB\, CNRS). \nEn français. \nLes présentations scientifiques sont ouvertes au personnel de Bordeaux Neurocampus. \nLes pauses café et le déjeuner sont réservés uniquement au personnel de Sanpsy\, merci de votre compréhension. \nTélécharger le programme (pdf) \n
URL:https://www.bordeaux-neurocampus.fr/en/event/symposium-sanpsy-2023/
CATEGORIES:For scientists,home-event,Symposium
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DTSTART;TZID=Europe/Paris:20230210T140000
DTEND;TZID=Europe/Paris:20230210T140000
DTSTAMP:20260602T022712
CREATED:20230130T114012Z
LAST-MODIFIED:20230130T120207Z
UID:154935-1676037600-1676037600@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Hongmei Zhu
DESCRIPTION:Venue: CGFB \nLanguage of defense: English \n\nTeam: Motoneurons and synaptic partners (MotoPSyn)\, INCIA\nThesis supervisor: Pascal Branchereau \nTitle\nPrenatal dysfunctions of chloride-related inhibition in lumbar motoneurons of the SOD1G93A ALS mouse model \nAbstract\nAmyotrophic lateral sclerosis (ALS) is a fatal and adult-onset neurodegenerative disease characterized by progressive degeneration of motoneurons (MNs) with complex multifactorial aetiology. Most ALS studies have focused on symptomatic stages based on the hypothesis that ALS pathogenesis occurs when the disease becomes symptomatic. However\, growing evidence indicates that ALS pathogenesis might start long before symptom onset. My PhD thesis work was based on the hypothesis that ALS – familial and sporadic – stems from deficits taking place during early development. With the aim of identifying early changes underpinning ALS neurodegeneration\, the first part of my thesis analysed the GABAergic/glycinergic inhibitory postsynaptic currents (IPSCs) to embryonic (E) E17.5 MNs located in the ventro-lateral motor column from SOD1G93A (SOD) mice\, in parallel with the analyse of chloride homeostasis. Our results showed that IPSCs are less frequent in SOD animals in accordance with a reduction of synaptic VIAAT-positive terminals in the close proximity of MN somata. SOD MNs exhibited an ECI 10 mV more depolarized than wild type (WT) MNs. This deficit in GABA/glycine inhibition was due to a reduction of the neuronal chloride transporter KCC2. SOD spontaneous IPSCs and evoked GABAAR-currents exhibited a slower decay correlated to elevated [Cl-]i. Using computer modelling approach\, we revealed that the slower relaxation of synaptic inhibitory events acts as a compensatory mechanism to strengthen or increase the efficacy of GABA/glycine inhibition when ECI is more depolarized. Interestingly\, simulations revealed an excitatory effect of low frequency (<50Hz) depolarizing GABA/glycine post-synaptic potentials (dGPSPs) in SOD-like MNs but not in WT-like littermates. At high frequency\, dGPSPs switched to inhibitory effect resulting from the summation of the shunting components. The second part of my PhD thesis focussed on the effect of electrically evoked-dGPSPs\, at different frequencies (7.5 to 100 Hz)\, on real lumbar E17.5 MNs in which a depolarized ECI (below spike threshold) was imposed. The aim was to examine whether the excitatory effect could be linked to morphological changes previously described in E17.5 SOD MNs. Results showed that some MNs were excited by low-frequency dGPSPs and inhibited by high-frequency dGPSPs (Dual MNs) and others were inhibited at all frequencies (Inhibited MNs). Dual effect was more often detected in SOD MNs. WT MNs were classified into two clusters according to their input resistance (Rin)\, Dual MNs being specific to high Rin and Inhibited MNs to low Rin. Morphometric data pointed out a reduced dendritic tree in high Rin WT Dual MNs and a large dendritic tree in low Rin Inhibited MNs. This was not the case in SOD MNs that were excited or inhibited whatever their morphology and Rin. In agreement with simulation showing that a less density of inhibitory current on MNs soma favors excitatory dGPSPs\, we found less synaptic VIAAT terminals on the soma and proximal dendrites of SOD MNs\, compared to littermate WT MNs\, as well as a lower frequency of spontaneous dGPSPs. Altogether\, my thesis data emphasize a prenatal defect in the Cl- homeostasis and GABA/glycine innervation in the SOD1G93A ALS MNs. Before birth\, a dominant population of MNs with low Rin emerges in WT animals. These MNs that are inhibited by dGPSPs could represent future ALS-vulnerable fast MNs (putative FF). Interestingly\, those MNs are not inhibited in SOD animals. The inhibitory dysfunction could be attributed to two distinct factors: morphology and perisomatic inhibitory synapse density. Of these two factors\, the latter plays a major role in controlling the capability of GABAergic/glycinergic neurons for shaping spinal motor output. \nKeywords: chloride homeostasis | synaptic integration | KCC2 | inhibition| spinal motoneurons| amyotrophic lateral sclerosis | SOD1G93A mouse model | simulation | patch-clamp | Prenatal stage | GABAergic/glycinergic synaptic transmission | GABA/glycine. \nPublications\nHongmei Zhu\, Urvashi Dalvi\, William Cazenave\, Daniel Cattaert and Pascal Branchereau. Excitatory action of low frequency depolarizing GABA/glycine synaptic events is favored in prenatal spinal SOD1G93A motoneurons. Submitted to Neurobiology of Disease. \nPascal Branchereau\, Elodie Martin\, Anne-Emilie Allain\, William Cazenave\, Laura Supiot\, Fara Hodeib\, Amandine Laupénie\, Urvashi Dalvi\, Hongmei Zhu\, Daniel Cattaert. Relaxation of synaptic inhibitory events as a compensatory mechanism in fetal SOD spinal motor networks. eLife\, 2019\, 8:e51402. \nJury\nMme Muriel Darnaudéry\nPr\, NutriNeurO\, Université de Bordeaux Présidente \nM. Daniel Zytnicki\nDR\, SPPIN\, Université Paris Cité Rapporteur \nM. Christophe Porcher\nPr\, INMED\, Université Aix-Marseille Rapporteur \nMme Sabine Lévi\nDR\, INSERM UMRS-1270\, Paris Examinateur \nM. Pascal Legendre\nDR\, INSERM U1130-CNRS UMR 8246-Sorbonne Université\, Paris Examinateur \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-hongmei-zhu/
CATEGORIES:Thesis
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