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Bordeaux School of Neuroscience

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  • C. Dejean et al. dans Neuropsychopharmacology

    13 févr. 2017

    le poids relatif des oscillations G60 / G80

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  • Conférence mensuelle - Christian Luscher

    3 mars 2017 à 11:30 - CGFB , Campus Carreire

    mechanisms that underlie the behavioral adaptation...

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  • Ronan Chereau, Valentin Nagerl et al. dans PNAS

    23 janv. 2017

    l’élargissement de l’arbre axonal induit...

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  • The Bordeaux Cell Biology Gathering Day

    4 avr. 2017

    Inscription gratuite maintenant....

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  • G.Marsicano, G.Ferreira et P.V Piazza et al. dans Molecular Psychiatry

    21 févr. 2017

    used to treat cannabis-induced psychotic-like stat...

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CRF1 receptor-deficiency increases cocaine reward.CRF1 receptor-deficiency increases cocaine reward.
Stimulant drugs produce reward but also activate stress-responsive systems. The corticotropin-releasing factor (CRF) and the related hypothalamus-pituitary-adrenal (HPA) axis stress-responsive systems are activated by stimulant drugs. However, their role in stimulant drug-induced reward remains poorly understood. Herein, we report that CRF1 receptor-deficient (CRF1-/-), but not wild-type, mice show conditioned place preference (CPP) responses to a relatively low cocaine dose (5 mg/kg, i.p.). Conversely, wild-type, but not CRF1-/-, mice display CPP responses to a relatively high cocaine dose (20 mg/kg, i.p.), indicating that CRF1 receptor-deficiency alters the rewarding effects of cocaine. Acute pharmacological antagonism of the CRF1 receptor by antalarmin also eliminates cocaine reward. Nevertheless, CRF1-/- mice display higher stereotypy responses to cocaine than wild-type mice. Despite the very low plasma corticosterone concentration, CRF1-/- mice show higher nuclear glucocorticoid receptor (GR) levels in the brain region of the hippocampus than wild-type mice. Full rescue of wild-type-like corticosterone and GR circadian rhythm and level in CRF1-/- mice by exogenous corticosterone does not affect CRF1 receptor-dependent cocaine reward but induces stereotypy responses to cocaine. These results indicate a critical role for the CRF1 receptor in cocaine reward, independently of the closely related HPA axis activity.
Contarino A, Kitchener P, Vallée M, Papaleo F, Piazza PV.
Neuropharmacology. 2017 Jan 27

Neuroinflammation in Autism: Plausible Role of Maternal Inflammation, Dietary Omega 3, and Microbiota.Neuroinflammation in Autism: Plausible Role of Maternal Inflammation, Dietary Omega 3, and Microbiota.
Several genetic causes of autism spectrum disorder (ASD) have been identified. However, more recent work has highlighted that certain environmental exposures early in life may also account for some cases of autism. Environmental insults during pregnancy, such as infection or malnutrition, seem to dramatically impact brain development. Maternal viral or bacterial infections have been characterized as disruptors of brain shaping, even if their underlying mechanisms are not yet fully understood. Poor nutritional diversity, as well as nutrient deficiency, is strongly associated with neurodevelopmental disorders in children. For instance, imbalanced levels of essential fatty acids, and especially polyunsaturated fatty acids (PUFAs), are observed in patients with ASD and other neurodevelopmental disorders (e.g., attention deficit hyperactivity disorder (ADHD) and schizophrenia). Interestingly, PUFAs, and specifically n-3 PUFAs, are powerful immunomodulators that exert anti-inflammatory properties. These prenatal dietary and immunologic factors not only impact the fetal brain, but also affect the microbiota. Recent work suggests that the microbiota could be the missing link between environmental insults in prenatal life and future neurodevelopmental disorders. As both nutrition and inflammation can massively affect the microbiota, we discuss here how understanding the crosstalk between these three actors could provide a promising framework to better elucidate ASD etiology.
Madore C, Leyrolle Q, Lacabanne C, Benmamar-Badel A, Joffre C, Nadjar A, Layé S.
Neural Plast. 2016. Review.

Social harassment induces anxiety-like behaviour in crayfish.Social harassment induces anxiety-like behaviour in crayfish.
Social interactions leading to dominance hierarchies often elicit psychological disorders in mammals including harassment and anxiety. Here, we demonstrate that this sequence also occurs in an invertebrate, the crayfish Procambarus clarkii. When placed in the restricted space of an aquarium, crayfish dyads generally fight until one of the opponents suddenly escapes, thereafter clearly expressing a submissive behaviour. Nevertheless, the winner frequently keeps on displaying excessive aggressive acts, having deleterious consequences in losers and interpreted as harassment behaviour. We indeed observed that, contrary to winners, losers expressed anxiety-like behaviour (ALB) in correlation with the stress intensity they suffered during the harassment period mainly. Injections of an anxiolytic abolished ALB, confirming its homology with anxiety. A serotonin (5-HT) antagonist had the same effect, suggesting a role for 5-HT, whose brain concentrations increased much more in losers than in winners. Our findings suggest that the bases of harassment and of its anxiogenic consequences have emerged very early during evolution, and emphasize crayfish as an unexpected but potentially fruitful model for the study of these social disorders.
Bacqué-Cazenave J, Cattaert D, Delbecque JP, Fossat P.
Sci Rep. 2017 Jan 3

Superresolution imaging reveals activity-dependent plasticity of axon morphology linked to changes in action potential conduction velocity.Superresolution imaging reveals activity-dependent plasticity of axon morphology linked to changes in action potential conduction velocity.
Axons convey information to nearby and distant cells, and the time it takes for action potentials (APs) to reach their targets governs the timing of information transfer in neural circuits. In the unmyelinated axons of hippocampus, the conduction speed of APs depends crucially on axon diameters, which vary widely. However, it is not known whether axon diameters are dynamic and regulated by activity-dependent mechanisms. Using time-lapse superresolution microscopy in brain slices, we report that axons grow wider after high-frequency AP firing: synaptic boutons undergo a rapid enlargement, which is mostly transient, whereas axon shafts show a more delayed and progressive increase in diameter. Simulations of AP propagation incorporating these morphological dynamics predicted bidirectional effects on AP conduction speed. The predictions were confirmed by electrophysiological experiments, revealing a phase of slowed down AP conduction, which is linked to the transient enlargement of the synaptic boutons, followed by a sustained increase in conduction speed that accompanies the axon shaft widening induced by high-frequency AP firing. Taken together, our study outlines a morphological plasticity mechanism for dynamically fine-tuning AP conduction velocity, which potentially has wide implications for the temporal transfer of information in the brain.
Chéreau R, Saraceno GE, Angibaud J, Cattaert D, Nägerl UV.
Proc Natl Acad Sci U S A. 2017 Feb 7


Les effets dopants de l'ANR

17 févr. 2017

..une étude vient pour la première fois, de quantifier l'effet de ces aides sur l'activité des chercheurs en France, les conclusions sont positives :...► Lire la suite

TDAH : une large étude d'imagerie trouve des anomalies cérébrales

17 févr. 2017

les personnes souffrant de TDAH ont des modifications de volumes de 5 des noyaux de la base du cerveau par rapport aux témoins, ce qui suggère que le ...► Lire la suite

Une mémoire cachée dans les synapses

8 févr. 2017

..une équipe américaine établit que l'activation neuronale n'est pas toujours indispensable à la mémoire de travail ► Lire la suite


Post-doc positions open / Team leader  
2-year postdoctoral position available in Neuroscience/Biological Psychiatry Laboratory of Nutrition and Integrative Neurobiology (NutriNeuro) Bordeaux...(January 2017)

Recherchons ! Bordeaux Neurocampus: 
en ligne le 19 sept 2016 ....Recherchons: Chef de projet du centre  d’excellence sur  les maladies neurodégénératives CHU de Bordeaux Hôpital Pellegrin - Institut des Maladies Neurodégénératives

 Recrutement PhD , ingénieurs , team leader etc...
SynDegen is currently able to offer 12 PhD student positions in the SynDegen ITN. Recrutons 2 thésards sur Bordeaux. Deadline pour les applications le 31 Janvier 2017…

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 Faculty of Health at Aarhus University, Call for applications........Proposition Poste MCU Poitiers : Le candidat travaillera dans l’équipe NeuroDéveloppement- NeuroAdaptation-NeuroDégénérescence au sein de l’UMR_S 1084 Inserm (LNEC)....




Maladie de Parkinson: de la cellule à l'humain...à Bordeaux


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