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:20230326T010000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20231029T010000
END:STANDARD
BEGIN:DAYLIGHT
TZOFFSETFROM:+0100
TZOFFSETTO:+0200
TZNAME:CEST
DTSTART:20240331T010000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20241027T010000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;VALUE=DATE:20230916
DTEND;VALUE=DATE:20240617
DTSTAMP:20260531T121556
CREATED:20230831T131841Z
LAST-MODIFIED:20240529T183442Z
UID:162245-1694822400-1718582399@www.bordeaux-neurocampus.fr
SUMMARY:Exposition : Cervorama
DESCRIPTION:Agitez vos neurones ! \nA travers cette exposition\, Cap Sciences propose aux visiteurs de découvrir le cerveau sous toutes ses formes lors d’une visite ponctuée de manipulations\, de jeux et d’expériences… Ils pourront notamment explorer les mondes des cerveaux de l’escargot\, l’abeille\, le singe et l’homme\, tester leur mémoire dans le “cognitilab”\, découvrir leur cerveau en 3D grâce au cervomaton ou encore analyser les capacités des animaux ! \nUne exposition conçue et réalisée par Cap Sciences en partenariat avec Bordeaux Neurocampus\n \nEn savoir plus\nSite web : https://www.cap-sciences.net/au-programme/exposition/grand-public/cervorama/ \n
URL:https://www.bordeaux-neurocampus.fr/en/event/exposition-cervorama/
CATEGORIES:Events for all,not-calendar,pour tous homepage,Semaine du cerveau 2024
END:VEVENT
BEGIN:VEVENT
DTSTART;VALUE=DATE:20231024
DTEND;VALUE=DATE:20231110
DTSTAMP:20260531T121557
CREATED:20221122T113608Z
LAST-MODIFIED:20231109T141649Z
UID:152946-1698105600-1699574399@www.bordeaux-neurocampus.fr
SUMMARY:Cajal lectures: Advanced techniques for synapse biology
DESCRIPTION:Venue: CGFB \nFree access \n\nOctober 24 – 9:00am \nCécile Charrier (Institute of Biology\, École Normale Supérieure\, France)\nMolecular mechanisms of synaptic development: insights from a human-specific gene. \nOctober 24 – 11:00am \nBrian Mac Cabe (EPFL\, Lausanne\, Swiss)\nUnknown knowns of Drosophila synapses. \nOctober 26 – 9:00am\n Noa Lipstein (LeibnizFMP\, Germany)\nSynaptic transmission in health and disease. \nOctober 26 – 11:00am\n Julie Perroy (IGF\, University of Montpellier\, France)\nMolecular dynamics at glutamatergic synapses and beyond. \nOctober 28 – 9:00am \nJosef Kittler (University College London\, UK)\nMolecular mechanism of inhibitory synapse formation and plasticity. \nOctober 30 – 9:00am \nDaniel Choquet (CNRS/University of Bordeaux\, France)\nNanoscale synapse organization and function. \nNovember 2 – 9:00am \nMarina Mikhaylova (Humboldt University \, Germany)\nCalcium and synaptic heterogeneity. \nNovember 3 – 9:00am\nRosa Paolicelli (University of Lausanne\, Swiss)\nMicroglia: key players in synapse remodeling in the healthy and diseased brain. \nNovember 3 – 11:00am \nAlfredo Kirkwood (Johns Hopkins University\, USA)\nPrinciples of Hebbian\, Pavlovian and Homeostatic synaptic plasticity. \nNovember 6 – 9:00am \nJuan Burrone (King’s College London\, UK)\nThe emergence and plasticity of inhibitory synapses: from dendrites to the axon initial segment. \nNovember 6 – 11:00am \nAxion BioSystems : Presentation \nNovember 7 – 9:00am \nNael Nadif Kasri (Radboud University Medical Center\, Netherlands)\nLeveraging spontaneous activity in human neuronal stem cell-derived neurons to model neurodevelopmental disorders. \nNovember 9 – 9:00am \nChristian Lohmann (Netherlands Institute for Neuroscience\, Netherlands)\nImaging synapse development. \nNovember 9 – 11:00am \nJulijana Gjorgjieva (Max Planck Institute for Brain Research\, Germany)\nEmergence of organization and computations at the subcellular and cellular scales. \nCourse directors\nAna Luisa Carvalho – Coimbra University\, Portugal \nMathieu Letellier – Bordeaux University\, France \nHey-Kyoung Lee – John Hopkins University.\, US \nAbout the course\nAdvanced techniques for synapse biology – CAJAL (cajal-training.org) \n
URL:https://www.bordeaux-neurocampus.fr/en/event/advanced-techniques-for-synapse-biology/
CATEGORIES:Cajal Lectures,For scientists
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20231103T113000
DTEND;TZID=Europe/Paris:20231103T113000
DTSTAMP:20260531T121557
CREATED:20230505T103506Z
LAST-MODIFIED:20231025T073258Z
UID:159231-1699011000-1699011000@www.bordeaux-neurocampus.fr
SUMMARY:Monthly conference (PhD seminar) - Claudia Verderio
DESCRIPTION:Venue: Centre Broca \n\nClaudia Verderio\nInstitute of Neurosciences\, Milan\, Italy \nInvited by Rebecca Hekking (Oliet’s team – Magendie) \nTitle\nMicroglial EVs travelling at the neuron surface: implication in synaptic pruning and abeta-related  synaptic dysfunction \nAbstract\nUsing optical tweezers combined to time-lapse imaging\, we studied EV-neuron interaction dynamics in vitro coming to the unexpected observation that a large fraction of glial EVs move along the surface of hippocampal neurons\, scanning actin protrusions (D’Arrigo et al.\, JEV 2021; Gabrielli et al.\, Brain 2022). In fully differentiated cultures\, EVs frequently stop moving at synaptic sites on dendrites\, while the fraction of moving EVs and average EV motion are elevated along axons. These data\, together with previous evidence showing that microglial EVs carry multiple signals implicated in synaptic pruning (PS\, complement factors)\, prompted us to investigate whether EVs may deliver molecules guiding microglia-mediated synaptic removal on dendrites and exploit axonal projections as highways to reach target neurons to spread pathological signals across the synapse. In my talk I go in deep into our research on these topics. \nThe hypothesis that EVs may use axons to move between synaptically connected neurons and spread their cargo was tested in a neurodegenerative context. According to our data\, the injection of large microglial EVs carrying Aβ species (Aβ-EVs) induces and propagates amyloid-related synaptic deficits among synaptically connected regions in a circuit primarily affected in Alzheimer’s disease (AD)\, i.e. the entorhinal-hippocampal circuit\, leading to progressive memory impairment and persistent network alterations both at hippocampal and cortical level (Gabrielli et. al\, Brain\, 2022; Falcicchia et al\, Brain Comm\, 2023). When the motility of Aβ-EVs is inhibited\, there is no synaptic dysfunction propagation nor network stability impairment. These data unveil motion of large Aβ-EVs at the neuron surface as a new mechanism contributing to the diffusion of Aβ-related pathology in AD. \nTo explore EV involvement in synaptic pruning\, we co-cultured neurons with wild type (wt) or mutant (C9orf72 knock out) microglia\, which produce more EVs and complement factors compared to wt\, and analyzed synaptic density\, finding that mutant microglia enhance engulfment of pre-synaptic material. Interestingly\, pretreatment of mutant microglia with GW4869\, an inhibitor of EV biogenesis\, restored normal pre-synaptic density\, while supplementation of microglial EVs to neurons decreased pre-synaptic density and favored engulfment of synaptic material/synaptosomes by microglia\, revealing that EVs promote synaptic pruning. Immunofluorescence analysis of C9orf72 ko hippocampi at P17 (peak synaptic pruning) showed lower density of Vglut+ pre-synapses and revealed higher C1q staining in CA1 area compared to wt\, linking larger EV production to enhanced C1q deposition and excessive pruning. \nOur studies shed light on the possible roles of microglial EVs in synaptic alterations in neurodevelopmental and neurodegenerative disorders. \nPublications\nD’Arrigo G\, Gabrielli M\, Scaroni F\, Swuec3 P\, Amin L\, Pegoraro A\, Adinolfi E\, Di Virgilio F\, Cojoc D\, Legname G\, Verderio C (2021) Astrocytes-derived extracellular vesicles in motion at the neuron surface: involvement of the prion protein. JEV\, Jul;10(9):e12114. \nGabrielli M\, Prada I\, Joshi P\, Falcicchia C\, D’Arrigo G\, Rutigliano G\, Battocchio E\, Zenatelli R\, Tozzi F\, Radeghieri A\, Arancio O\, Origlia N* and Verderio C* (2022) Microglial large extracellular vesicles propagate early synaptic dysfunction in Alzheimer’s disease. Brain\, 45(8):2849-2868. \nFalcicchia C\, Tozzi F\, Gabrielli M\, Amoretti S\, Masini G\, Nardi G\, Guglielmo S\, Ratto GM\, Arancio O\, Verderio C*\, Origlia N* (2023)(*co-corresponding author). Microglial extracellular vesicles induce Alzheimer’s disease-related cortico-hippocampal network dysfunction. Brain Commun. May 31;5(3): fcad170. doi: 10.1093/braincomms/fcad170. \n\nPhD seminars are organized by the NBA\, Bordeaux Neurocampus\, and the Bordeaux Neurocampus Graduate Program \n
URL:https://www.bordeaux-neurocampus.fr/en/event/monthly-conference-phd-seminar-november2023/
CATEGORIES:For scientists,home-event,Monthly conferences
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20231103T140000
DTEND;TZID=Europe/Paris:20231103T140000
DTSTAMP:20260531T121557
CREATED:20230926T132921Z
LAST-MODIFIED:20231030T111405Z
UID:162608-1699020000-1699020000@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Zoé Grivet
DESCRIPTION:Venue : Centre Broca \nThesis defense in french \n\nZoé Grivet\nIMN\nTeam : Monoamines\, Parkinson and Pain\nThesis directed by Pascal Fossat\n \n\nTitle\nInvolvement of serotonergic descending pathways in the control of nociception in Parkinson disease \nAbstract\nParkinson disease (PD) is a multi-factory disorder leading to motor but also to non-motor symptoms\, associated with dopamine (DA) depletion in basal ganglia. One of the major non-motor symptom is chronic pain whose underlying mechanisms are still largely unknown. Beyond DA\, it is also known that other monoaminergic systems such as serotonergic (5-HT) are altered in PD. Moreover\, 5-HT descending neurons projecting from the nucleus raphe magnus (NRM) to the dorsal horn of the spinal cord (DHSC) exert an important pain modulation. Thus\, we hypothesized that chronic pain in PD is associated to a perturbation of pain control by 5-HT descending pathways. To test this\, we used the 6-OHDA mouse model of PD that kill over 90% of DA neurons in the SNc. Depletion of DA neurons led to decreased bilateral mechanical pain thresholds and increased nociceptive activity in the dorsal horn of the spinal cord (DHSC) notably by inducing a hyperactivity of spinal nociceptive neurons. Additionally\, we found an increased activity of 5-HT neurons of the nucleus raphe magnus\, an increased barrage of excitatory inputs on these neurons and raised 5-HT levels in the spinal cord compared to sham animals. To verify that the observed hypersensitivity in 6-OHDA mice was directly linked to the increased 5-HT activity\, we used transgenic mice expressing cre-recombinase in 5-HT neurons\, allowing specific expression of light-dependent inhibitory opsins. Inhibition of the 5-HT-spinal cord pathway partially restored pain sensitivity in 6-OHDA animals and reduced nociceptive activity in the DHSC. This partial recovery could be mimicked by intrathecal injection of 5-HT2a and 5-HT3 receptor antagonists. These results show that DA depletion is associated to increase 5-HT neuron activity in the NRM that mediate spinal hyperexcitability associated to nociceptive hypersensitivity. These results show a 5-HT facilitatory pathway after DA depletion. In contrast\, previously\, in naive mice we showed a 5-HT descending pain inhibition suggesting that the role of serotonin in nociceptive control change upon 5-HT neurons activity. To test for that hypothesis\, we thus investigated the role of the level of stimulation of the 5-HT descending pathway on nociceptive response and dorsal horn neurons excitability. We show that contrary to DA depletion\, inhibition of 5-HT pathways reduced paw withdrawal thresholds and increased nociceptive neuron activity in the DHSC\, demonstrating a tonic anti-nociceptive role of the 5-HT pathway under normal conditions. Next\, we activated 5-HT descending pathways using different optogenetic and chemogenetic protocols of stimulation. We confirmed with optogenetic that short-term stimulation of 5-HT neuron is analgesic while longer stimulation are proalgesic. Chemogenetic experiments also suggest different DCZ concentrations also lead to opposite pain control but experiments need to be consolidated. However\, all these results support the hypothesis that the activity level of 5-HT neurons controls their effect on nociceptive transmission from antinociceptive at low level to pronociceptive at higher levels. We finally address the question of the spinal 5-HT receptors involved and we show that analgesic effect is associated to activation of local inhibitory interneurons expressing 5-HT2a and c receptors while hyperalgesic effect of high level of activity need the recruitment of 5-HT3 receptors. \nIn conclusion\, this work demonstrates that (1) the level of activity of 5-HT neurons is a crucial indicator of serotonergic control of pain going from analgesia to hyperalgesia\, and that (2) the loss of DA neurons in PD leads to increased activity of 5-HT descending pathway\, resulting in a spinal 5-HT2a/5-HT3 dependent nociceptive hypersensitivity in mice. Lastly\, it opens avenues for exploring the use of serotonin antagonists in the potential treatment of chronic pain in Parkinson’s disease and the use 5-HT neurons activity as an indicator of pathological pain. \nKey words\nNociception\, Serotonin\, Parkinson disease\, Spinal cord\n \nJury\nFOSSAT Pascal\, Professeur\, Université de Bordeaux – Directeur de thèse\nMme COIZET Véronique\, Chargée de recherche\, GIN\, Grenoble – Rapporteure\nBARROT Michel\, Directeur de recherche\, INCI\, Strasbourg – Rapporteur\nFRANCOIS Amaury\, Chargé de recherche\, IGF\, Montpellier – Examinateur\nMme. BERTRAND Sandrine\, Directrice de recherche\, INCIA\, Bordeaux – Examinatrice\nMme. BEYELER Anna\, Chargée de recherche\, Neurocentre Magendie – Examinatrice \nPublications\nAby\, F.\, Lorenzo\, L. E.\, Grivet\, Z.\, Bouali-Benazzouz\, R.\, Martin\, H.\, Valerio\, S.\, … & Fossat\, P. (2022). Switch of serotonergic descending inhibition into facilitation by a spinal chloride imbalance in neuropathic pain. Science Advances\, 8(30)\, eabo0689.\nDOI : 10.1126/sciadv.abo0689\nWinke\, N.\, Aby\, F.\, Jercog\, D.\, Zoé\, G.\, Girard\, D.\, Landry\, M.\, … & Herry\, C. (2022). Brainstem somatostatin-expressing cells control the emotional regulation of pain behavior. bioRxiv\, 2022-01\nhttps://doi.org/10.1101/2022.01.20.476899 \n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-zoe-grivet/
CATEGORIES:Thesis
END:VEVENT
END:VCALENDAR