Seminars
07/04/2021 09h00
Steve DOS SANTOS CARVALHO, 3rd Bordeaux Cell Biology Gathering
2021-04-07 09:00:00 2021-04-07 18:00:00 Europe/Paris Steve DOS SANTOS CARVALHO, 3rd Bordeaux Cell Biology Gathering 0    Show the web article Link

Lieu: Agora du Haut Carré, Talence

Join us and participate in the third BCBG meeting occuring at Talence (Agora Du Haut Carré) on April the 7th of 2020.

Program available here


Pour plus de détails: https://neurocentre-magendie.fr/NCM_Downloads_open/BCBG2020Programme.pdf


Seminars
14/02/2020 11h30
Chantal Mathis

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.




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

MetaboDay aims at promoting interactions between researchers of the Bordeaux area interested in the various aspects of metabolism. This scientific event is open to researchers, post-docs and PhD students from all fields.

Registration is free but mandatory.


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


Seminars
24/01/2020 11h30
Francisco Papaleo

Lieu: Centre Broca Nouvelle-Aquitaine

from IIT Central Research Labs Genova's lab will give a presentation entitled '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

Invited by Giovanni Marsicano (Neurocentre Magendie)

Summary:

The prefrontal cortex (PFC) has been implicated in processing of the emotional state of others through nonverbal communication. This social cognitive function is altered in psychiatric disorders such as autism and schizophrenia and is hypothesized to rely on an intact cortical neuronal excitatory and inhibitory balance. Here, by combining in vivo electrophysiology with a behavioral task for emotion recognition in mice, we show that neurons in the medial prefrontal cortex (mPFC) are differentially activated during exploration of conspecifics depending on their affective state. Optogenetic manipulations revealed a double dissociation of interneuron roles in emotion recognition; specifically, inhibition of mPFC somatostatin (SOM+) but not of parvalbumin (PV+) interneurons abolishes emotion discrimination. Conversely, activation of mPFC SOM+ interneurons induces social discrimination in this task. Our findings provide new insights into the neurobiological mechanisms of emotion recognition.



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

Lieu: Médiathèque Jacques Ellul de Pessac


Par Véronique Pallet (NutriNeuro) et Blandine Cherifi (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

Organised by: Maurice Garret – Nathalie Sans – Mathieu Letellier


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


Seminars
03/05/2019 14h00
Dr. Julia Lemos, Dissecting the actions of CRF in the NAc
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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/


Seminars
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.

Selected publications

– Minocha, S., Valloton, D., Brunet, I., Eichmann, A., Hornung, J.-P., Lebrand, C., (2015), NG2 glia are required for vessel network formation during embryonic development. Elife 4.

– Aspalter, I.M., Gordon, E., Dubrac, A., Ragab, A., Narloch, J., Vizán, P., Geudens, I., Collins, R.T., Franco, C.A., Abrahams, C.L., Thurston, G., Fruttiger, M., Rosewell, I., Eichmann, A., Gerhardt, H., (2015). Alk1 and Alk5 inhibition by Nrp1 controls vascular sprouting downstream of Notch. Nat Commun 6, 7264.

– Fortuna, V., Pardanaud, L., Brunet, I., Ola, R., Ristori, E., Santoro, M.M., Nicoli, S., and Eichmann, A. (2015). Vascular Mural Cells Promote Noradrenergic Differentiation of Embryonic Sympathetic Neurons. Cell Rep 11, 1786–1796.

– Rama N., Dubrac A., Mathivet T., Ní Chárthaigh R.-A., Genet G., Cristofaro B., Pibouin-Fragner L., Ma L., Eichmann A. & Chédotal A. (2015), Slit2 signaling through Robo1 and Robo2 is required for retinal neovascularization. Nat. Med. 21, 483–491.


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


Seminars
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