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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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TZID:Europe/Paris
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DTSTART:20230326T010000
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DTSTART:20231029T010000
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DTSTART:20240331T010000
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BEGIN:VEVENT
DTSTART;VALUE=DATE:20230916
DTEND;VALUE=DATE:20240617
DTSTAMP:20260531T172129
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
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BEGIN:VEVENT
DTSTART;VALUE=DATE:20231024
DTEND;VALUE=DATE:20231110
DTSTAMP:20260531T172129
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
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20231107T093000
DTEND;TZID=Europe/Paris:20231107T123000
DTSTAMP:20260531T172129
CREATED:20230927T092906Z
LAST-MODIFIED:20231103T105041Z
UID:162643-1699349400-1699360200@www.bordeaux-neurocampus.fr
SUMMARY:Mini-symposium "Molecular and cellular mechanisms of synapse physiology"
DESCRIPTION:Venue : Centre Broca Nouvelle-Aquitaine \n\nProgramme\n9:30 – Maria Passafaro\nTitle : Unraveling PCDH19-related pathogenic mechanisms in Developmental and Epileptic Encephalopathy 9 (DEE9) \nAbstract \nMutations in PCDH19 gene\, which encodes protocadherin-19 (PCDH19)\, cause Developmental and Epileptic Encephalopathy 9 (DEE9). Heterogeneous loss of PCDH19 expression in neurons is considered a key determinant of the disorder; however\, how PCDH19 mosaic expression affects neuronal network activity and circuits is largely unclear. Here\, we show that the hippocampus of Pcdh19 mosaic mice is characterized by structural and functional synaptic defects and by the presence of PCDH19-negative hyperexcitable neurons. Furthermore\, a global reduction of network firing rate and increased neuronal synchronization has been observed in different limbic system areas. Finally\, network activity analysis in freely behaving mice revealed a decrease in excitatory/inhibitory ratio and functional hyperconnectivity within the limbic system of Pcdh19 mosaic mice. Altogether\, these results indicate that altered PCDH19 expression profoundly affects circuit wiring and functioning and provide new key to interpret DEE9 pathogenesis. \n\n10:10 – Andrea Barberis\nTitle : Spatial determinants for the interactions of glutamatergic and GABAergic synapses in dendrites of hippocampal pyramidal neurons \nAbstract \nTraditionally\, plasticity was considered to belong mostly to excitatory synapses while inhibitory transmission was assumed to be relatively invariant. However\, recent evidences demonstrate several types of inhibitory synaptic plasticity\, raising the important question of how GABAergic and glutamatergic synaptic plasticity are coordinated during neuronal activity. We investigated how synaptic plasticity induced at individual glutamatergic spines affects the strength of neighboring GABAergic synapses. To this end we induced “single spine LTP” by pairing the postsynaptic depolarizations with repetitive glutamate uncaging at individual spines while simultaneously measuring the strength of adjacent dendritic GABAergic synapses by GABA uncaging. We found that\, after the induction of single-spine LTP\, GABAergic synapses located within 3 micrometers from a potentiated spine showed depression (iLTD)\, while further synapses still showed iLTP. This “spread” of heterosynaptic plasticity from spines was dependent on the protease activity of calpain induced by calcium influx through L-type voltage gated calcium channels. Presently we are extending the study of the aforementioned plasticity short range interplay at specific hippocampal CA3-CA1 sub-circuits. Our findings show that both glutamatergic and GABAergic synaptic plasticity are finely coordinated at dendritic level suggesting that the dendritic E/I ratio can be selectively tuned in spatially restricted dendritic sub-regions. In this scenario\, the unique distribution of dendritic excitatory and inhibitory inputs and the consequent plasticity interplay is expected to influence the non-linear dendritic input summation thus efficiently tuning the neuronal excitability. \n\n10:50 – Kirill Volynski\nTitle : Synergistic regulation of neurotransmitter release by different synaptotagmin isoforms. \n\n11:30 – Aude Panatier\nTitle: Astrocytic EphB receptors control NMDAR functions and memory \nAbstract \nThe activation of classical NMDA receptors (NMDARs) requires the binding of glutamate and of a co-agonist. d-serine released from astrocytes is acting as such a co-agonist at several central synapses. In the hippocampus\, while d-serine is the co-agonist of synaptic NMDARs\, glycine is the one at extra-synaptic sites. The close apposition of astrocytic processes with synaptic neuronal elements could be an interesting signal for synaptic release of d-serine. Interestingly\, it has been shown in astrocytic cultures that astrocytic EphB3 receptors play a role in the synthesis and release of D-serine. However\, we do not know whether it could impact synaptic NMDAR activity. Here\, we first established that the stimulation of EphB receptors by exogenous ephrinB3 led to an increase of d-serine availability at CA3-CA1 synapses\, inducing an increase of NMDAR activity. Importantly\, the inhibition of endogenous EphB receptors impaired NMDAR activity. These effects depended on astrocytes as EphB3 receptors activation by exogenous ephrinB3 had no impact on NMDAR activity under conditions where calcium activity was inhibited specifically in astrocytes. Finally\, the knock down of EphB3 receptors specifically in astrocytes lead to LTP and novel object recognition memory impairment\, both rescued by exogenous d-serine. Altogether our data indicate that astrocytic EphB3 receptors play a key role in synaptic NMDAR functions and memory. \n\n14:00 : PhD defense of Agata NowackaDifferential contributions of pre- and postsynaptic components in tuning high-frequency short-term synaptic plasticity \nMore details \nOrganized by Daniel Choquet \n
URL:https://www.bordeaux-neurocampus.fr/en/event/seminar-molecular-and-cellular-mechanisms-of-synapse-physiology/
CATEGORIES:For scientists,home-event,Symposium
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20231107T093000
DTEND;TZID=Europe/Paris:20231107T123000
DTSTAMP:20260531T172129
CREATED:20231004T122749Z
LAST-MODIFIED:20231004T122749Z
UID:163058-1699349400-1699360200@www.bordeaux-neurocampus.fr
SUMMARY:Mini-symposium "Molecular and cellular mechanisms of synapse physiology"
DESCRIPTION:Venue : Centre Broca Nouvelle-Aquitaine \n\nProgramme\n9h30 – Maria PassafaroUnraveling PCDH19-related pathogenic mechanisms in Developmental and Epileptic Encephalopathy 9 (DEE9) \n10h10 – Andrea BarberisSpatial determinants for the interactions of glutamatergic and GABAergic synapses in dendrites of hippocampal pyramidal neurons \n10h50 – Kirill VolynskiSynergistic regulation of neurotransmitter release by different synaptotagmin isoforms. \n11h30 – Aude PanatierAstrocytic EphB receptors control NMDAR functions and memory \nAnd \n14h – PhD defense of Agata NowackaDifferential contributions of pre- and postsynaptic components in tuning high-frequency short-term synaptic plasticity \n
URL:https://www.bordeaux-neurocampus.fr/en/event/mini-symposium-molecular-and-cellular-mechanisms-of-synapse-physiology/
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20231107T140000
DTEND;TZID=Europe/Paris:20231107T140000
DTSTAMP:20260531T172129
CREATED:20230921T072657Z
LAST-MODIFIED:20230921T074017Z
UID:162532-1699365600-1699365600@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Agata Nowacka
DESCRIPTION:Venue : Centre Broca Nouvelle-Aquitaine  \nThesis defense in English \n\nAgatha Nowacka\nIINS\nTeam : Dynamic organization and function of synapses\nThesis director : Daniel Choquet \n\nTitle\nDifferential contributions of pre- and postsynaptic components in tuning high-frequency short-term synaptic plasticity \nAbstract\nActivity-dependent plasticity of synaptic transmission is a key mechanism underlying learning and memory. During high-frequency short-term synaptic plasticity (HF-STP)\, the amplitude of synaptic responses changes upon presynaptic stimulation on a timescale of milliseconds. HF-STP is important for information processing in the brain\, serving particularly for temporal integration. However\, the precise functions of HF-STP\, and its impact on information processing\, remain unknown. It is widely accepted that HF-STP is regulated primarily by presynaptic mechanisms. However\, postsynaptic mechanisms have been shown to also regulate HF-STP\, although their role here remains to be fully understood. Previously\, we demonstrated that AMPA receptors (AMPARs)\, the main excitatory receptors in the brain\, are trafficked between the extrasynaptic and synaptic compartments through surface diffusion that complements endo- and exocytosis. Here\, I studied the functional role of AMPAR surface diffusion in HF-STP in integrated slice tissue models with intact synaptic connectivity. I use the AP-GluA2 knock-in (KI) mouse model\, we developed\, where GluA2 subunits of AMPARs are tagged with a 15 amino acid biotinylation acceptor peptide (AP-tag) and can be specifically biotinylated when co-expressed with an endoplasmic reticulum resident biotin ligase (BirAER)\, and immobilized on the cell surface with a biotin-binding protein NeutrAvidin. Using this toolset\, I show that immobilization of endogenous AMPARs modulates HF-STP by increasing synaptic depression in the Schaffer collateral-CA1 synapse of organotypic hippocampal slices. This effect is reversed when AMPAR desensitization blockers are applied\, suggesting that the modulation of HF-STP is achieved by preventing the replacement of desensitized AMPARs in the synapse. Moreover\, when imaging glutamate release with the iGluSnFr sensor we find no change in presynaptic glutamate release upon AMPAR immobilization. Altogether this strongly suggests a postsynaptic contribution of AMPAR mobility in regulating HF-STP. Surprisingly\, AMPAR cross-link has no effect on HF-STP in SC-CA1 synapses in ex vivo brain slices. Next\, I demonstrate that AMPAR immobilization strongly increases synaptic depression in the L4-L2/3 synapse in the primary somatosensory cortex (S1) of ex vivo brain slices\, with no consecutive change in glutamate release measured with iGluSnFR. We find that the rate of AMPAR surface diffusion is higher in the L2/3 than CA1 synapses. This points to a synapse-specific effect of AMPAR mobility on shaping HF-STP that depends on the mutual contribution of presynaptic glutamate release\, AMPAR desensitization and surface diffusion. I demonstrate that GSG1L\, an AMPAR auxiliary protein expressed highly in the cortex but not CA1\, can regulate AMPAR surface diffusion and HF-STP. Next\, we show that AMPAR mobility tunes synaptic calcium integration and network activity. Finally\, we demonstrate that AMPAR immobilization downstream of paCaMKII activation and LTP induction results in increased synaptic depression in intact tissue. In the last part of the project\, I show that AMPAR immobilization can also produce an opposing effect and promote synaptic facilitation\, an effect found in juvenile SC-CA1 synapse as well as the lateral perforant path to granule cell synapse in the adult dentate gyrus. This finding further emphasizes the synapse and development specific effects of AMPAR immobilization on HF-STP. Altogether\, I determined the respective contributions of presynaptic transmitter release\, postsynaptic AMPAR biophysics and mobility in HF-STP and identified physiological processes which act upon AMPAR kinetics and mobility to regulate HF-STP in the brain. Moreover\, AMPAR cross-link is a promising tool to achieve cell-specific blockade of HF-STP that may allow the transition from modeling-based evidence of HF-STP roles in brain function to experimental evidence. \nKey words\nAMPAR\, AMPAR surface diffusion\, short-term synaptic plasticity\, synaptic integration \nJury\nDr. Aude Panatier\, Neurocentre Magendie\nDr. Maria Passafaro\, Università di Milano\nDr. Andrea Barberis\, Instituto Italiano di Tecnologia\nDr. Kirill E. Volynski\, University College London\nDr. Daniel Choquet\, IINS \nPublications\nZiółkowska M\, Borczyk M\, Cały A\, Tomaszewski KF\, Nowacka A\, Nalberczak-Skóra M\, Śliwińska MA\, Łukasiewicz K\, Skonieczna E\, Wójtowicz T\, Wlodarczyk J\, Bernaś T\, Salamian A\, Radwanska K. Phosphorylation of PSD-95 at serine 73 in dCA1 is required for extinction of contextual fear. PLoS Biol. 2023; 21(5):e3002106. doi: 10.1371/journal.pbio.3002106. \nKuzniewska B\, Rejmak K\, Nowacka A\, Ziółkowska M\, Milek J\, Magnowska M\, Gruchota J\, Gewartowska O\, Borsuk E\, Salamian A\, Dziembowski A\, Radwanska K\, Dziembowska M. Disrupting interaction between miR-132 and Mmp9 3’UTR improves synaptic plasticity and memory in mice. Front Mol Neurosci. 2022. doi: 10.3389/fnmol.2022.924534. \nGetz\, A.M.\, Ducros\, M.\, Breillat\, C.\, Lampin-Saint-Amaux\, A.\, Daburon\, S.\, François\, U.\, Nowacka\, A.\, Fernández-Monreal\, M.\, Hosy\, E.\, Lanore\, F.\, Zieger\, H.\, Sainlos\, M.\, Humeau\, Y.\, Choquet\, D. High-resolution imaging and manipulation of endogenous AMPA receptor surface mobility during synaptic plasticity and learning. Sci Adv\, 2022. 8(30): p. eabm5298. \nNowacka\, A.\, Borczyk\, M.\, Salamian\, A.\, Wojtowicz\, T.\, Wlodarczyk\, J. & Radwanska\, K. 2020. PSD-95 Serine 73 phosphorylation is not required for induction of NMDA-LTD. Scientific Reports. 2020. doi:10.1038/s41598-020-58989-2 \nNowacka\, A.\, Borczyk\, M. Ketamine applications beyond anesthesia – A literature review. European Journal of Pharmacology. 2019. doi:10.1016/j.ejphar.2019.172547 \nSzczałuba\, K.\, Chmielewska\, J.J.\, Sokołowska\, O.\, Rydzanicz\, M.\, Szymańska\, K.\, Feleszko\, W.\, Włodarski\, F.\, Biernacka\, A.\, Murcia Pieńskowski\, W.\, Walczak\, A.\, Bargeł\, E.\, Królewczyk\, K.\, Nowacka\, A.\, Stawiński\, P.\, Nowis\, D.\, Dziembowska\, M.\, Płoski\, R. Neurodevelopmental phenotype caused by a de novo PTPN4 single nucleotide variant disrupting protein localization in neuronal dendritic spines. Clinical Genetics. 2018. 94(6): 581-585. \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-agata-nowacka/
CATEGORIES:Thesis
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