Les dernières actualités

Comme chaque année, de nombreux ateliers sont proposés par les équipes du centre pour permettre aux lycéens de découvrir l'univers de la recherche et l'environnement du laboratoire.

Le Neurocentre Magendie Inserm Université de Bordeaux s'engage pour une Recherche Inclusive 365 jours/an.

La demie finale de ma thèse en 180 secondes c’est mardi prochain, et le Neurocentre y sera.
Venez soutenir Ashley !!!
Ça se passe au Haut-Carré de Talence.

27/02/2019 10h00
Kamila CASTRO from Frick's lab will give a presentation entitled 'Brain network and Autism Spectrum Disorder'

27/02/2019 10h30
Zoe HUSSON from Cota's lab will give a presentation entitled "Role of the POMC-ventral striatal neurocircuit in the development of diet- induced obesity"

27/02/2019 11h00
Zhe ZHAO from Marsicano's lab will give a presentation entitled “Role of the cannabinoid receptor type 1 in the control of water intake”.

15/02/2019 11h30
Isabelle Brunet, Collège de France - Molecular Control of Neuro-Vascular Development
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Lieu: CGFB Seminar room

Invitant : Mireille Montcouquiol (Neurocentre Magendie, Montcouquiol-Sans's lab)

Sympathetic arterial innervation and EphrinaA4/EPHA4 Signaling: Arteries under pressure?


Arteries receive a sympathetic innervation which is crucial to control their contraction level. Sympathetic nerves establish „“en passant““ synapses, called neurovascular junctions with arterial smooth muscle cells. Gene expres- sion comparison of non-innervated and innervated arteries revealed that the re- pulsive axon guidance molecule EphrinA4 is surprisingly expressed by arteries ar the onset of innervation (Postnatal day 2 P2). We here investigated the role of EphrinA4 signalization in the development and physiology of arterial innervation in mice. We showed that EphrinA4 is expressed by smooth muscle cells of resistance arteries and identified its receptor EphA4, expressed by sympathetic neurons. Binding and collapse experiments showed that EphrinA4 mediates the collapse of sympathetic growth cones in vitro via EphA4. EphrinA4 KO and EphA4 KO mice exhibited an increased arterial innervation at P2, consistent with a loss of repulsion. We then generated EphA4 flox-TH CRE mice who exhibited the same enhanced arterial innervation at P2 , which remained in adult mice. Increased arterial innervation in EPhA4 flox-TH CRE mice was correlated with a higher number of neurovascular junctions and a modifcation of their structure visible by eletronic microscopy. Measurement of cutaneous blood flow using laser doppler revealed an enhanced vasoconstriction in this mice. Resistivity and pulstility index of ca- rotids calculated from ultrasound views were increased, suggesting enhanced vascular resistivity. Thus EphrinA4 expressed by arterial smooth muscles cells induces collapse of sympathetic growth cones via the receptor EphA4 to refine sympathetic arterial innervation. Impairment of EphrinA4/EphA4 signaling leads to increased arterial innervation, vascular resistance and vasoconstriction. As systemic blood pressure depends on cardiac output but also vascular resistance, we are currently testing if those functional defects could lead to hypertension from sympathetic origin, or at least aggravate pre-existing hypertension.

Pour plus de détails: https://www.college-de-france.fr/site/en-cirb/brunet.htm

08/02/2019 11h30
Sandrine Humbert, Grenoble Institut des Neurosciences – INSERM U836 – UGA
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Lieu: Amphi CGFB

Sandrine Humbert, Grenoble Institut des Neurosciences – INSERM U836 – UGA will give a presentation entitled 'Is Huntington disease –a late onset neurological condition- a neurodevelopmental disorder?'

Invitants : Maurice Garret de l’INCIA et Nathalie Sans du Neurocentre Magendie

Huntington 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.

Selected publications
Barnat 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.
Thion 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.
Elias 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.
Molina-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.
Elias 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.

Pour plus de détails: https://neurosciences.univ-grenoble-alpes.fr/fr/recherche/equipes-de-recherche/equipe-progeniteurs-neuraux-et-pathologies-cerebrales--637944.htm?RH=NEUROFR_RECHEQUI

30/01/2019 10h00
Yamuna MARIANI from Marsicano's lab will give a presentation entitled "Role of striatonigral and striatopallidal CB1 receptors in the physiology of Basal Ganglia."

30/01/2019 10h30
Nadia DI FRANCO from Revest's lab will give a presentation entitled "CB1 in Down Syndrome: a new potential target"