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Séminaire
19/10/2018 11h30
Cendra Agulhon
2018-10-19 11:30:00 2018-10-19 12:30:00 Europe/Paris Cendra Agulhon 0    Afficher l'article web Link

Lieu: Amphi du Centre Broca

Group Leader from Paris Descartes University - Team Interactions Glie-Glie and Glie-Neurones in Neurophysiopathology's lab will give a presentation entitled 'Contributions of astrocyte and satellite signaling to sensory processing'


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2018/cendra-agulhon.html


Séminaire
04/10/2018 11h30
Michel Baudry
2018-10-04 11:30:00 2018-10-04 12:30:00 Europe/Paris Michel Baudry 0    Afficher l'article web Link

Lieu: Amphi du Centre Broca

from Dean, Graduate College of Biomedical Sciences Western University of Health Sciences (Pomona, CA USA)'s lab will give a presentation entitled 'Opposite functions of calpain-1 and calpain-2 in the brain'

Invitant : Daniel Choquet, Team Leader: Dynamic organization & Function of synapses / Directeur de l'IINS


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2018/michel-baudry.html


Info générale
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Le prochain congrès « Aging 2018 » se tiendra au domaine du Haut Carré à Talence du 26 au 28 septembre 2018. Il réunira les membres de la communauté neuroscientifique internationale autour d’un thème central : le vieillissement cognitif en absence de MA et l’existence de différences inter-individuelles dans l’atteinte mnésique au cours de l’âge.

Invitant : Bordeaux Neurocampus, Gwenaelle Catheline, Aline Marighetto, Nora Abrous
L’inscription est obligatoire pour toute personne participant ou assistant au Congrès. La soumission d’un abstract ne peut se faire qu’après inscription. Le colloque accueillera un maximum de 280 personnes. Les participants sont tenus d'être présents durant les 3 jours.





Séminaire
25/09/2018 14h00
Sophie TRONEL

Lieu: Neurocentre Magendie Seminar room

Soutenance HDR: Sophie Tronel from Abrous's lab will give a presentation entitled 'Etude de la stabilisation de la mémoire'



Séminaire
21/09/2018 11h30
Jason Shepherd, University of Utah - Host Anna Beyeler
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Lieu: Amphithéâtre du Centre Broca Nouvelle-Aquitaine

Inter-cellular RNA transfer: a novel role of the neuronal gene Arc which encodes a repurposed retrotransposon protein

The neuronal gene Arc is essential for long-lasting information storage in the mammalian brain. We recently found that Arc self-assembles into virus-like capsids that encapsulate RNA. Endogenous Arc protein is released from neurons in extracellular vesicles that mediate the transfer of Arc mRNA into new target cells. These results show that Arc exhibits similar molecular properties to retroviral Gag proteins. Evolutionary analysis indicates that Arc is derived from a vertebrate lineage of Ty3/gypsy retrotransposons, which are also ancestors to retroviruses. These findings suggest that Gag retroelements have been repurposed during evolution to mediate intercellular communication in the nervous system. Our working model posits that Arc protein is locally translated in dendrites, where it forms a capsid that binds local mRNAs that are transported out of the cell.



Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2018/jason-shepherd.html



L'article Hippocampal CB1 Receptors Control Incidental Associations, une collaboration Bordeaux Neurocampus a fait l'objet d'un abstract video publié sur la chaine de Neuron, à voir ici : https://youtu.be/1qF2NUBylhA





Lieu: Amphi du Centre Broca

Dr. Marloes Henckens from Department of Cognitive Neuroscience, Donders Institute for Brain (Netherlands)'s lab will give a presentation entitled 'The neural signature of trauma susceptibility'

Invitant : Aline Desmedt, PhD , Maitre de Conférence au Neurocentre Magendie, Team Marighetto 'Pathophysiology of declarative memory'

Posttraumatic stress disorder (PTSD) is a psychiatric disorder which can develop after exposure to a traumatic event. Flashbacks, spontaneous recollection and recurrent nightmares of the trauma are amongst the most devastating symptoms of PTSD, through which patients continuously relive their trauma. Interestingly, only a small fraction (8-10%) of all trauma-exposed individuals eventually develops PTSD, whereas the rest is resilient and remains healthy. But how is the vulnerable brain different from the resilient one and when do these differences arise? Understanding the mechanisms behind these inter-individual differences could contribute to new clinical intervention strategies.
The use of a mouse model for PTSD allows us to study the mechanisms underlying relative resilience or susceptibility to PTSD in a longitudinal fashion, under controlled settings, while allowing for more invasive brain measurements. In this model, mice are first exposed to a traumatic event (i.e., severe unpredictable foot shock), followed by a trigger (i.e., mild predictable foot shock) in a different context one day later. Following a week of recovery, eventual development of PTSD-like symptomatology is assessed using a battery of behavioural tests to identify mice resilient and vulnerable to the trauma. Combining this model with functional MRI obtained both before and after trauma exposure, allowed us to study the development of a potential imbalance in neural network function as a consequence of trauma in the PTSD-vulnerable vs resilient brain, as well as the potential presence of neural abnormalities prior to trauma exposure in these animals. To study brain responses to the trauma itself, we used the so-called targeted recombination in active populations (TRAP) mice, in which the injection of tamoxifen opens up a temporal window in which all neurons expressing certain immediate early genes (reflecting neuronal activity), are permanently fluorescently labelled. We injected these animals with tamoxifen just prior to trauma exposure, and again assessed PTSD-symptoms later on. By re-exposing them to the traumatic context just before sacrifice and analysing trauma retrieval-induced neuronal activity by immunohistochemistry, we were moreover able to analyse the storage of the trauma memory into long-term memory. This allowed us to assess whether aberrant storage of the trauma memory could explain the emotional hypermnesia and contextual hypomnesia of the trauma that seem to characterize PTSD patients.


Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2018/marloes-henckens.html



Busquets-Garcia A, Oliveira da Cruz J, Terral G, Pagano Zottola AC, Soria-Gómez E, Contini A, Martin H, Redon B, Varilh M, Ioannidou C, Drago F, Massa F, Fioramonti X, Trifilieff P, Ferreira G*, Marsicano G* (2018).Hippocampal CB1 receptors control incidental associations. Neuron https://doi.org/10.1016/j.neuron.2018.08.014





Le travail des AP du centre a fait l'objet d'une interview publiée dans le N° du mois d'aout de la lettre Objectif Santé & Sécurité de l'Inserm.
Lire l'interview en page 3.





En page 6 du magazine, Émilie décrit ses découvertes sur le rôle de la protéine CaMKII dans la modulation de la migration neuronale. L'article peut être consulté ici : https://fr.calameo.com/read/005154450616c517dbd2a