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Dix ans pour mettre au point une gélule qui peut changer la vie de beaucoup d'addicts, une vie qui peut tourner au cauchemar.
C'est un travail d'équipe au long cours qui a ses racines à Bordeaux. Au cours de ses recherches sur les effets du canabis, l'équipe du Neurocentre Magendie a découvert que sa prise entraîne la production dans le cerveau d’une molécule appelée prégnénolone. Elle a pour effet naturel de défendre l’organisme contre les effets de cette drogue. Une solution pour soigner l'addiction au cannabis. Impossible de l'utiliser en tant que telle, elle ne s'y prête pas. Les chercheurs, fédérés autour de Pier-Vincenzo Piazza, directeur de recherche Inserm, ont donc trouver la parade...





Notre publication parue en Avril 2017 dans Nature Communications porte sur un nouveau rôle de la
protéine Gpsm2 dans le contrôle de la dynamique du cytosquelette d’actine. Elle est relayée par le
Magazine Sciences et Santé de l'Inserm.




Press review
07/09/2016
La publication de l'équipe de Cyril Herry dans Nature relayée par Sciences et Santé
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L'équipe de Cyril Herry publie une nouvelle fois ses travaux dans Nature. La publication de juillet 2016 porte sur les mécanismes de l'expression de la peur dans le cortex préfrontal dors médian. Elle est relayée par le Magazine Sciences et Santé de l'Inserm.





Erwan Bézard, directeur de l'IMN, est à l'honneur dans le magazine de l'Inserm pour ses travaux sur les maladies neurodégénératives.
Retrouvez la vidéo que la Fédération Bordeaux Neurocampus lui consacrait ici : https://youtu.be/RM-O2D44s8E





Nature. 2016 Jul 21;535(7612):420-4.
Prefrontal neuronal assemblies temporally control fear behaviour.
Dejean C, Courtin J, Karalis N, Chaudun F, Wurtz H, Bienvenu TC, Herry C.

Over the past decades, numerous studies demonstrated a critical role of the medial prefrontal cortex (mPFC) in regulation emotional behaviour, in particular learned fear responses. In these studies, in which the neuronal substrates of aversive learning were investigated, encoding of fear behavior was assumed to rely on the activity of single neurons through a rate coding mechanism in which the sole firing rate determine the behavioral output. This form of neuronal cording is strongly limited by the fact that over long distances, rate codes are not optimal for the fast information transmission that is required for rapid behavioural adaptation when facing threatening stimuli. In addition to this rate coding mechanism, neurons with different and specific firing sequences may cooperate and collectively provide information, a phenomenon referred to as "temporal coding".

In temporal coding, precise timing of firing is important, whereas average firing rates can remain stable. Assemblies of neurons enable temporal coding, and one of its obvious advantages is its great flexibility. Thus, neurons might rapidly switch between multiple functional networks according to sensory and internal inputs and determine specific behavioral outputs. Brain oscillations are thought to be instrumental in temporal coding by binding cell assemblies, organizing individual firing into meaningful collective activity, and coordinating remote areas. Whereas temporal coding has been described for sensory processing and spatial learning, its role in encoding emotional behaviour is virtually unknown.

To address this question we use a combination of single-unit and local field potential recordings along with optogenetic manipulations to show that, in the dmPFC, expression of conditioned fear is causally related to the organization of neurons into functional assemblies. During fear behaviour, the development of 4 Hz oscillations coincides with the activation of assemblies nested in the ascending phase of the oscillation. The selective optogenetic inhibition of dmPFC neurons during the ascending or descending phases of this oscillation blocks and promotes conditioned fear responses, respectively. These results identify a novel phase-specific coding mechanism, which dynamically regulates the development of dmPFC assemblies to control the precise timing of fear responses.





Fear response to traumatic or threatening situations helps us evade or escape danger. At the same time fear response is learned in the form of association between stimulus or situation and the presence of a stressor. This association is very powerful and leaves a memory trace that persists for years after a single experience, generating profound structural and functional changes in the brain that can potentially develop into post-traumatic stress and other anxiety-related disorders.




Press review
04/02/2016
Retour sur le Grand Prix Inserm 2015
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Un article du N°29 de 'Sciences et Santé' est consacré au Grand Prix Inserm de Piervi.




Press review
04/02/2016
Aline Desmedt dans 'Sciences et Santé'
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Pour les survivants et les témoins des attaques terroristes qui ont frappé
Paris le 13 novembre 2015, il existe un risque de développer des séquelles
psychologiques, et notamment un trouble de stress post-traumatique.
Certains sont-ils plus à risque que d’autres ? Quels marqueurs permettent
très tôt de les identifier, et ainsi de mieux les prendre en charge ?
Quel est l'avis d'Aline Desmedt ?




Press review
16/01/2016
Existe-t-il une vulnérabilité individuelle face à l'addiction ? - PierVi sur BFM Business







Cocaine taking behavior: CB1 receptors in Glu and GABA neurons don’t play the same role.

The endocannabinoid system acts on brain regions involved in reinforcement and addiction to drugs of abuse such as cocaine. The CB1 receptor is the main component of the endocannabinoid system and plays a key role in these processes. So far, however, CB1 receptors have been globally targeted, independent of their localization on specific neuronal populations, including glutamatergic or GABAergic neurons, generating controversial and potentially biased results. Here we demonstrate that the control exercised by CB1 receptors over cocaine taking behavior is differential depending on their localization in glutamatergic or GABAergic neurons. Thus, CB1 receptors in glutamatergic neurons control associative learning through which environmental stimuli gain control over drug seeking while CB1 receptors located on GABAergic neurons control the sensitivity to the primary rewarding effects of the drug.

Differential Control of Cocaine Self-Administration by GABAergic and Glutamatergic CB1 Cannabinoid Receptors.
Martín-García E, Bourgoin L, Cathala A, Kasanetz F, Mondesir M, Gutiérrez-Rodriguez A, Reguero L, Fiancette JF, Grandes P, Spampinato U, Maldonado R, Piazza PV, Marsicano G, Deroche-Gamonet V.  Neuropsychopharmacology. 2015 Nov 27. doi: 10.1038/npp.2015.351.