Les dernières actualités

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

Lieu: Amphi Broca

Principal Investigator, Momentum Laboratory of Molecular Neurobiology,Budapest , Hungary, Hungarian Academy of Sciences - Synaptic junctions are major sites of communication in the brain, where chemical messenger molecules transmit information from presynaptic neurons to their postsynaptic partners.The efficacy of synaptic transmission is not constant in time and space. Instead, its plasticity is a fundamental phenomenon underlying information storage and adaptation to environmental stimuli. Although classical neurotransmitters (such as glutamate and GABA) have well characterized principal roles in mediating basal neurotransmission, emerging evidence has revealed that synapses exploit a plethora of additional messenger molecules integrated into sophisticated signaling pathways to accomplish their complex functions. Thus, the major objective of our laboratory is to identify new signaling systems regulating synaptic transmission and its plasticity. We aspire to delineate the molecular architecture of these novel pathways and to elucidate their physiological roles. Ultimately, this activity is envisaged to help gain a better understanding of synaptic function and reveal new aspects of impaired synaptic activity in brain disorders.

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2019/istvan-katona.html

11/01/2019 11h30
Stefano Palminteri invited by Véronique Deroche-Gamonet
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Lieu: Amphi CGFB

Humans are biased reinforcement learners: evidence from behavioural and neural data

Abstract : The goal of a reinforcement learner is learning what to do so as to maximize future expected reward. A prerequisite to achieve this goal is to learn a action value function, that is an internal estimation of the future expected reward following a given action. In this talk I will present behavioural and neural evidence that humas do not learn this action value function in an objective manner.

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2019/stefano-palminteri.html

13/12/2018 10h00
Olfaction Symposium - organized by Guillaume Ferreira, Lisa Roux & Giovanni Marsicano
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Lieu: Neurocentre Magendie Seminar Room

Si l’olfaction a longtemps été considéré comme une sensorialité « secondaire » de nombreuses découvertes récentes, en particulier sur le fonctionnement cérébral, l’ont remis sur le devant de la scène. Les différents conférenciers illustreront lors d’une première session les bases neurobiologiques qui permettent ces importantes capacités d’apprentissages olfactifs (Busquets-Garcia, Nicole), aussi bien chez l’animal que chez l’homme, et ce dès la naissance (Coureaud, Sullivan). Lors d’une seconde session, les intervenants se focaliseront sur la physiologie des premiers relais cérébraux de traitement de l’information olfactive, à savoir le bulbe olfactif et le cortex piriforme (ou leurs équivalents chez la drosophile) ainsi que leurs étroites interactions (Nissant, Plaçais, Martin et Wilson).

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

05/12/2018 10h00
Vladimir Ivosev, invited by Anna Beyeler
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Lieu: Neurocentre Magendie Seminar room

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Pour plus de détails: https://en.vectorbuilder.com/

27/11/2018 11h00
Abel Eraso Pichot (Autonomous University of Barcelona)

Lieu: Neurocentre Magendie Seminar room

- Adaptive regulation of calcium excitability and energy metabolism by CREB-dependent transcription in astrocytes: study of the mechanisms governing astrocyte plasticity

An increasing body of evidence suggests that astrocytes participate in higher-brain functions, controlling from synaptic transmission to global brain waves and learning and memory processes. Different mechanisms have been proposed to mediate these astrocyte-dependent processes, astrocytic lactate release and calcium-dependent gliotransmission being the main known effectors. The existence of control of brain functions by astrocytes suggests that astrocytes may shape brain functions in response to experience as much as neurons, thus constituting the phenomenon of astrocyte plasticity. In neurons, the transcription factor CREB is the best known coordinator of synaptic and intrinsic plasticity. The fact that, in astrocytes, CREB activation is also activity-dependent, positions CREB as an ideal target to promote plasticity-related changes in astrocytes, too. In this study, we have analyzed the effect of the activation of CREB-dependent transcription in astrocytes, specifically regarding calcium signals and metabolism. We have demonstrated that activation of CREB-dependent transcription reduces cytosolic calcium events via mitochondria and increases lactate release, which may have impact on synaptic transmission. An important contribution of the study is the molecular analysis of astrocytic mitochondria, which has revealed that astrocytes may use fuels other than glucose such as fatty acids to meet basic energy metabolic demands. Taken together, our results establish astrocytic CREB as a hub in astrocyte-plasticity and shed light on the interplay between plasticity and energy metabolism in astrocytes.

13/11/2018 14h00
Jean-Sébastien Jouhanneau

Lieu: CGFB - Salle de conférence

Mécanismes synaptiques de tir épars

Lieu: Amphi du Centre Broca Nouvelle-Aquitaine

de l'Institut Curie (Paris) fera une présentation intitulée 'Microtubule-based transport in radial glial progenitor cells'. Conférence mensuelle - PhD seminar series
Invitant : Bordeaux Neurocampus / NBA

Pour plus de détails: http://www.bordeaux-neurocampus.fr/fr/manifestations-scientifiques/seminaires-2018/alexandre-baffet-phd-series.html

Lieu: Amphi du Centre Broca

Chef de groupe de l'Université Paris Descartes - Equipe Interactions Glie-Glie et Glie-Neurones dans le laboratoire de Neurophysiopathologie fera une présentation intitulée 'Contributions des astrocytes et de la signalisation satellite au traitement sensoriel'.

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