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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:20240331T010000
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DTSTART:20241027T010000
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DTSTART;VALUE=DATE:20240708
DTEND;VALUE=DATE:20240713
DTSTAMP:20260422T175449
CREATED:20231110T091644Z
LAST-MODIFIED:20240712T142744Z
UID:164270-1720396800-1720828799@www.bordeaux-neurocampus.fr
SUMMARY:Neuroergonomics
DESCRIPTION:Venue: Campus Victoire\, Bordeaux \n\nThe 5th International Neuroergonomics Conference will be held on July 8-12\, 2024\, following the success of the previous Neuroergonomics editions. \nThe 2024 Neuroergonomics Conference showcases a wide range of neurotechnologies. These advancements cover diverse areas\, including critical care\, well-being\, and everyday life. The spectrum of innovations presented includes revolutionary invasive devices\, targeted non-invasive approaches\, and wearable technologies. \nThe conference explores how these technologies benefit various fields\, such as enhancing the performance of human operators\, impaired patients\, elderly or athletes. Moreover\, it delves into cutting-edge concepts like brain-computer interfaces\, neurofeedback\, neurostimulation\, or mixed/virtual reality. By incorporating a diverse lineup of speakers and topics\, the 2024 Neuroergonomics program fosters a meeting culture that encourages the exchange of fresh ideas and facilitates meaningful connections. \nLocal organizing committee\nCamille Jeunet (CNRS\, INCIA – Equipe Mococo)\nFabien Lotte (Inria – Equipe Potioc) \nMore details\nWebsite: https://neuroergonomics2024.inria.fr/ \n
URL:https://www.bordeaux-neurocampus.fr/en/event/neuroergonomics/
CATEGORIES:For scientists,Symposium
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BEGIN:VEVENT
DTSTART;VALUE=DATE:20240709
DTEND;VALUE=DATE:20240710
DTSTAMP:20260422T175449
CREATED:20241216T160805Z
LAST-MODIFIED:20241216T160805Z
UID:178910-1720483200-1720569599@www.bordeaux-neurocampus.fr
SUMMARY:Soutenance de thèse - Alice Napias
DESCRIPTION:\nSommeil et mémoire associative verbale : Relation entre le sommeil évalué en vie quotidienne et la reconnaissance mnésique de paires de mots concrets et abstraits chez les jeunes adultes étudiants et perspectives chez les adultes âgés \n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-alice-napias/
CATEGORIES:Thesis
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20240709T140000
DTEND;TZID=Europe/Paris:20240709T140000
DTSTAMP:20260422T175449
CREATED:20240613T164911Z
LAST-MODIFIED:20240701T151451Z
UID:172717-1720533600-1720533600@www.bordeaux-neurocampus.fr
SUMMARY:Soutenance de thèse - Celeste Ferraguto
DESCRIPTION:Venue: centre Broca \nDefense in french \n\nCeleste Ferraguto\nTeam: “MEMORY”\, INCIA \nSupervisor: Susanna Pietropaolo \nTitle\nBKCa channels as therapeutic targets in neurodevelopmental disorders: focus on acoustic dysfunction \nAbstract\n\nNeurodevelopmental disorders (NDDs) are typically characterized by a range of pathological phenotypes\, encompassing a variety of physical\, brain and behavioral abnormalities. Among these\, impaired auditory perception and hearing alterations are commonly observed across multiple NDDs. Given the presence of a shared symptomatology\, increasing interest is devoted to the identification of potential common underlying mechanisms and\, therefore\, shared therapeutic strategies. Despite extensive efforts\, effective pharmacological interventions for most NDDs are still lacking\, prompting research on novel drugs\, as well as on repurposed treatments. Dysfunction in big conductance calcium-activated potassium (BKCa) ion channels has emerged as a potential key pathological mechanism involved in multiple NDDs: these ubiquitous channels play a pivotal role in modulating the activity of excitable cells\, including neurons\, vascular smooth-muscle and cardiac cells\, as well as cochlear hair cells\, thus being strongly implicated in synaptic\, cardio-vascular and auditory functions. Notably\, reduced expression and functionality of BKCa channels have been documented in patients with two major NDDs\, i.e.\, fragile X and Williams-Beuren syndromes (FXS and WBS)\, suggesting that compounds activating these channels could offer promising treatments for these two genetic syndromes. This thesis aimed to provide preclinical evidence supporting the therapeutic potential of chlorzoxazone\, an FDA-approved BKCa channel opener\, for treating the pathological phenotypes of FXS and WBS. To this end\, we employed the Fmr1-KO and the CD mouse lines\, representing the main preclinical models of FXS and WBS\, respectively\, which recapitulate most symptoms displayed by patients\, including BKCa channel expression and functional deficits. In the first part of the thesis\, we demonstrated that chlorzoxazone\, administered either acutely or chronically\, effectively treated various behavioral\, brain\, and physical phenotypes exhibited by Fmr1-KO and CD mutants. To this aim\, we combined behavioral assessments of both mutant mouse lines\, encompassing motor\, emotional\, and social tests\, with the analysis of markers of neuronal plasticity and functionality markers\, e.g.\, dendritic abnormalities\, neurotrophin levels\, and fos expression in specific brain regions. Additionally\, in the CD mouse model\, we characterized cardiovascular phenotypes typical of WBS\, i.e.\, cardiac hypertrophy and aortic stenosis. In the second part\, we focused on the auditory alterations displayed by the two mouse models and we showed the overall efficacy of chlorzoxazone in rescuing these abnormalities at electrophysiological\, structural\, and behavioral levels. This involved assessing auditory brainstem responses and distortion product otoacoustic emissions\, alongside the immuno-histochemical evaluation of cochlear hair cells and ribbon synapses\, and behavioral analysis of the acoustic startle response. Overall\, our findings support BKCa channels as promising therapeutic targets for FXS and WBS\, as well as for associated auditory dysfunctions. Furthermore\, they advocate for repurposing chlorzoxazone\, already on the market for muscular pathologies\, for clinical use in the context of NDDs. In conclusion\, this thesis provides a preclinical foundation for future clinical trials in FXS and WBS\, and encourages further preclinical research into the role of BKCa channels in auditory and behavioral dysfunction. \nKeywords: Neurodevelopmental disorders\, BKCa channels\, auditory impairments\, genetic mouse models\, pharmacology\, mouse behaviour \nPublications\nC. Ferraguto\, Y. Bouleau\, T. Peineau\, D. Dulon\, S. Pietropaolo. Hyperacusis in the Adult Fmr1-KO Mouse Model of Fragile X Syndrome: The Therapeutic Relevance of Cochlear Alterations and BKCa Channels. Int J Mol Sci. 2023 Jul 24;24(14):11863. doi: 10.3390/ijms241411863. \nS. Giannoccaro*\, C. Ferraguto*\, V. Petroni\, C. Marcelly\, X. Nogues\, V. Campuzano\, S.Pietropaolo. Early Neurobehavioral Characterization of the CD Mouse Model of Williams-Beuren Syndrome. Cells. 2023 Jan 21;12(3):391. doi: 10.3390/cells12030391. * equal contribution \nI. Del Pino\, C.Tocco\, E. Magrinelli\, A. Marcantoni\, C. Ferraguto\, G. Tomagra\, M. Bertacchi\, C. Alfano\, X.Leinekugel\, A. Frick\, M. Studer. COUP-TFI/Nr2f1 Orchestrates Intrinsic Neuronal Activity during Development of the Somatosensory Cortex. Cereb Cortex. 2020 Oct 1;30(11):5667-5685. doi: 10.1093/cercor/bhaa137. \nJury\nMme. BARDONI Barbara Directrice de Recherche\, Université Côte d’Azur\, Rapporteur \n EL-AMRAOUI Aziz Directeur de Recherche Université Paris Cité\, Institut Pasteur\, Rapporteur \n BONNARD Damien MCU-PH\, Université de Bordeaux\, Examinateur \n DELPECH Jean-Christophe Chargée de Recherche\, Université de Bordeaux\, Examinateur \n DULON Didier Directeur de Recherche\, Université de Bordeaux\, Invité \n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-celeste-ferraguto/
CATEGORIES:Thesis
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