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X-WR-CALNAME:Bordeaux Neurocampus
X-ORIGINAL-URL:https://www.bordeaux-neurocampus.fr
X-WR-CALDESC:Évènements pour Bordeaux Neurocampus
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TZID:Europe/Paris
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TZOFFSETFROM:+0100
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TZNAME:CEST
DTSTART:20190331T010000
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TZNAME:CET
DTSTART:20191027T010000
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20190208T110000
DTEND;TZID=Europe/Paris:20190208T120000
DTSTAMP:20260504T224641
CREATED:20190204T173303Z
LAST-MODIFIED:20200316T134729Z
UID:102907-1549623600-1549627200@www.bordeaux-neurocampus.fr
SUMMARY:Séminaire impromptu : Bastien Berret
DESCRIPTION:Lieu : salle de réunion de l’INCIA \nBastien Berret\n(Université Paris-Sud\, http://hebergement.u-psud.fr/berret/ ) \nInvitant : Aymar de Rugy\nINCIA \nAbstract: In daily life we often move at a self-selected pace\, thereby choosing certain relationships between amplitude\, speed or duration\, i.e. movement vigor. Yet\, the principles underlying the formation of movement vigor remain unclear. If basal ganglia dysfunction clearly affects movement vigor\, as exemplified by bradykinesia in Parkinson’s patients\, relatively large inter-individual differences have also been reported among healthy participants performing various motor tasks such as saccades\, walking or reaching. Biomechanics (e.g. anthropometry) likely contributes to inter-individual differences but recently a “cost of time” theory has been proposed to be the cornerstone of such differences in movement invigoration. It assumes that the brain puts a cost on time during the neural control of movement. In this talk\, I will review earlier theories that have been proposed to account for the vigor of human movement and motivate the cost of time theory as a normative means to predict the vigor of self-paced arm movements. The proposed theory can account for the formation of movement vigor as well as for inter-individual differences beyond simple biomechanical discrepancies. The consistency of the cost of time across modeling choices\, tasks or repeated measurements will then be explored\, and future works will be discussed. Overall\, the formation of vigor is a central (yet still intriguing) aspect of human motor behavior that seems to require a multidisciplinary approach lying at the interface of mathematics\, biomechanics\, neurophysiology and psychology\, to be better understood. \n
URL:https://www.bordeaux-neurocampus.fr/event/seminaire-impromptu-bastien-berret/
CATEGORIES:A la une,Pour les scientifiques,Séminaire Impromptu
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DTSTART;TZID=Europe/Paris:20190208T113000
DTEND;TZID=Europe/Paris:20190208T130000
DTSTAMP:20260504T224641
CREATED:20190102T172651Z
LAST-MODIFIED:20190204T174530Z
UID:101219-1549625400-1549630800@www.bordeaux-neurocampus.fr
SUMMARY:Séminaire - Sandrine Humbert
DESCRIPTION:Sandrine Humbert\nLieu CGFB \nSandrine Humbert\nDR INSERM\, team leader: Équipe « Progéniteurs neuraux et pathologies cérébrales » Grenoble Institut des Neurosciences – INSERM U836 – UGA \nInvitants : Maurice Garret de l’INCIA et Nathalie Sans du Neurocentre Magendie \n\nAbstract :\nHuntington Disease (HD) belongs to the family of late onset manifesting neurological disorders including Alzheimer and Parkinson diseases. The cause of HD is the presence of an abnormal expansion of a polyglutamine tract in the huntingtin (HTT) protein. HD is characterized by a long premanifest phase before onset of progressive neurological and psychiatric symptoms at adult age\, yet mutant HTT (mHTT) is expressed from the very beginning of life. Anyway\, given the adult onset and dysfunction and death of adult neurons characterizing HD\, most studies have focused on the toxic effects elicited by mutant HTT in post-mitotic neurons and the roles of the wild-type protein during development have been overlooked. We will discuss how HTT regulates several steps of mouse embryonic corticogenesis. HTT is crucial to maintain the pool of cycling progenitors and for the migration and post-natal maturation of post-mitotic neurons. We will describe the underlying molecular mechanisms by which HTT mediates its effects. Finally\, we will also show the consequences of the presence of an abnormal polyglutamine expansion in HTT during cortical neurogenesis and consider the viewing of HD as a developmental disorder. \n\nSelected publications\nBarnat M\, Le Friec J\, Benstaali C and Humbert\, S (2017). Huntingtin-mediated Multipolar-Bipolar Transition of Newborn Cortical Neurons is Critical for their Postnatal Neuronal Morphology. Neuron\, 93\, 99-114. \nThion MS\, McGuire JR\, Sousa CM\, Fuhrmann L\, Fitamant J\, Leboucher S\, Vacher S\, Tezenas du Montcel S\, Bièche I\, Bernet A\, Patrick Mehlen P\, Anne Vincent-Salomon A\, and Humbert\, S (2015). Unravelling the role of huntingtin in breast cancer metastasis. J. Natl. Cancer Inst.\, doi: 10.1093/jnci/djv208. \nElias S\, McGuire JR\, Yu H and Humbert S (2015). Huntingtin is required for epithelial polarity through RAB11A mediated apical trafficking of PAR3-aPKC. Plos Biol.\, 13:e1002142. \nMolina-Calavita M\, Barnat M\, Elias S\, Aparicio E\, Piel M and Humbert S (2014). Mutant huntingtin affects cortical progenitor cell division and development of the mouse neocortex. J. Neurosci.\, 34\, 10034-10040. \nElias S\, Thion MS\, Yu H\, Moreira Sousa C\, Lasgi C\, Morin X and Humbert S (2014). Huntingtin Regulates Mammary Stem Cell Division and Differentiation. Stem Cell Reports\, 2\, 491-506. \n\n\n
URL:https://www.bordeaux-neurocampus.fr/event/seminaire-sandrine-humbert/
LOCATION:CGFB\, 38 rue Albert Marquet\, Bordeaux\, 33000\, France
CATEGORIES:Séminaire du vendredi
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