Séminaire
07/04/2020 09h00
Steve DOS SANTOS CARVALHO, 3rd Bordeaux Cell Biology Gathering
2020-04-07 09:00:00 2020-04-07 18:00:00 Europe/Paris Steve DOS SANTOS CARVALHO, 3rd Bordeaux Cell Biology Gathering 0

Lieu: Agora du Haut Carré, Talence

Rejoignez nous et participez au 3ème BCBG qui aura lieu à Talence (Agora du Haut Carré) le 7 Avril 2020



Séminaire
14/02/2020 11h30
Chantal Mathis
2020-02-14 11:30:00 2020-02-14 12:30:00 Europe/Paris Chantal Mathis 0

Lieu: Neurocentre Magendie Seminar room

from DR2 CNRS, LNCA, Strasbourg's lab will give a presentation entitled 'Early memory deficits appearing during preclinical stages in mouse models of Alzheimer disease'

Invited by Nora Abrous (Neurocentre Magendie)

Abstract

Over the last decade, the main finding about Alzheimer’s disease (AD) is that initial signs have been detected 15 to 20 years before diagnosis (e.g., see Bateman et al, 2012 and Jack et al, 2009). Since then, a great deal of efforts concentrated on the identification of early events and biomarkers that might help us to understand AD pathogenesis. The nature and severity of recognition deficits evolve as AD pathology spreads through medial temporal lobe networks and connected brain structures playing a key role in recognition memories. Therefore, object recognition paradigms have been useful to determine early memory deficits in animal models of AD. The pertinence of behavioral data provided by these paradigms will be analyzed in regard to the neuropathological phenotype of genetically modified rodent models of AD. Our aim is to outline clear advantages and possible limitations in their translational value. We propose that future progress depends on understanding neural networks supporting each form of recognition memory in parallel with the improvement of animal models of AD.



Séminaire
30/01/2020 09h00
MetaboDay
2020-01-30 09:00:00 2020-01-30 18:00:00 Europe/Paris MetaboDay 0    Afficher l'article web Link

Lieu: Agora du Domaine du Haut-Carré (Talence)

MetaboDay vise à favoriser les interactions entre les chercheurs de la région bordelaise intéressés par les différents aspects du métabolisme. Cette manifestation scientifique est ouverte aux chercheurs, post-docs et doctorants de tous horizons.

L'inscription est gratuite mais obligatoire.


Pour plus de détails: www.tbmcore.u-bordeaux.fr/metabo-day/


Séminaire
24/01/2020 11h30
Francisco Papaleo

Lieu: Centre Broca Nouvelle-Aquitaine

du laboratoire IIT Central Research Labs Genova donnera une présentation intitulé "Bottom-Up and Top-Down Control of Emotion Recognition"

Francisco Papaleo
Senior Researcher Tenure Track – Principal Investigator
IIT Central Research Labs Genova
https://www.iit.it/people/francesco-papaleo

Invité par Giovanni Marsicano (Neurocentre Magendie)

Résumé:
Le cortex préfrontal (PFC) a été impliqué dans le traitement de l'état émotionnel des autres par la communication non verbale. Cette fonction cognitive sociale est altérée dans les troubles psychiatriques tels que l'autisme et la schizophrénie et on suppose qu'elle repose sur un équilibre cortical neuronal excitateur et inhibiteur intact. Ici, en combinant l'électrophysiologie in vivo avec une tâche comportementale de reconnaissance des émotions chez la souris, nous montrons que les neurones du cortex préfrontal médian (mPFC) sont activés de manière différentielle lors de l'exploration des congénères en fonction de leur état affectif. Des manipulations optogénétiques ont révélé une double dissociation des rôles des interneurones dans la reconnaissance des émotions ; plus précisément, l'inhibition des interneurones de la somatostatine (SOM+) du mPFC mais pas de la parvalbumine (PV+) abolit la discrimination des émotions. Inversement, l'activation des interneurones mPFC SOM+ induit une discrimination sociale dans cette tâche. Nos résultats apportent de nouvelles connaissances sur les mécanismes neurobiologiques de la reconnaissance des émotions.



Séminaire
23/01/2020 18h30
Conférence : « Déséquilibre alimentaire : quelles conséquences »

Lieu: Médiathèque Jacques Ellul de Pessac


Par Véronique Pallet (NutriNeuro) et Blandine Cherifi (Equipe Cota - Neurocentre Magendie)

Animé par Thierry Amédée (IINS)





Lieu: Auditorium Médiathèque Jacques Ellul – Pessac

from Marsicano's lab will give a presentation entitled 'Sport : quand la motivation dépasse la raison'


Pour plus de détails: https://www.bordeaux-neurocampus.fr/event/conference-a-pessac/



Lieu: Auditorium Centre Broca Nouvelle Aquitaine

Organisé par: Maurice Garret – Nathalie Sans – Mathieu Letellier


Pour plus de détails: https://www.bordeaux-neurocampus.fr/en/journee-synapse/


Séminaire
03/05/2019 14h00
Dr. Julia Lemos, Dissecting the actions of CRF in the NAc
   Afficher l'article web Link

Lieu: Amphi Centre Broca

Dr. Julia Lemos is an Assistant Professor at the Department of Neuroscience of the University of Minnesota (USA) and will present the work of her lab dissecting the actions of corticotropin releasing factor (CRF) in the nucleus accumbens.
Host: Anna Beyeler

Outside of its well-characterized actions in the HPA axis, the stress-associated peptide corticotropin-releasing factor (CRF) regulates neuronal excitability and synaptic transmission in several extrahypothalamic brain regions. Previous research has shown that CRF in the nucleus accumbens (NAc) promotes appetitive behavior through mechanisms that remain poorly understood. We have recently showed that CRF potentiates both dopaminergic and cholinergic transmission in the NAc. However, it is unknown how CRF regulates the activity of medium spiny neurons (MSNs), the principle projection neurons of the NAc, to modulate behavioral output. MSNs are classified by their peptide expression and projection targets within the basal ganglia: dMSNs form the direct projection pathway and express dynorphin, whereas iMSNs form the indirect pathway and express enkephalin. RNAscope in situ hybridization was used to assess Crh1 mRNA expression in MSN subpopulations, identifying dMSNs and iMSNs with expression of dynorphin (pdyn) or enkephalin (pEnk), respectively. 20% of all cells were positive for Crh1 mRNA, with approximately 30% co-expressing pEnk mRNA (iMSNs), 30% co-expressing pDyn mRNA (dMSNs) and 30% co-expressing neither marker. Using whole-cell patch clamp electrophysiology recordings in brain slices, we examined the function of exogenously-applied CRF on the excitability of MSNs in the NAc core. Application of 100 nM CRF produced a leftward shift in the current-voltage relationship, demonstrating that CRF can enhance the firing rate of both dMSNs and iMSNs. Next steps will focus on identifying the role of CRF receptor subtypes in enhancing the spiking activity in MSNs and elucidate whether this effect is through direct actions on MSNs or through dopaminergic and cholinergic modulation of MSNs.


Pour plus de détails: https://www.lemoslaboratory.org/


Séminaire
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?

Abstract

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


Séminaire
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