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 :

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.

Revue de presse
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.

Revue de presse
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 ?

Revue de presse
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. 

L’Italie, bien sûr : cet accent coloré, ce goût du rire, cette élégance de l’habit et de l’esprit… Mais aussi la Sicile, terre volcanique et stratégique, de sécession parfois. De son île natale, Pier Vincenzo Piazza a hérité une allure et un tempérament. Il y mêle une touche personnelle, faite d’exigence intellectuelle et d’opiniâtreté. « Pier Vincenzo Piazza a l’allure du Sud et la rigueur du Nord », résume le professeur Amine Benyamina, psychiatre, responsable du Centre d’addictologie de l’hôpital Paul-Brousse à Villejuif (Val-de-Marne).

Mardi 8 décembre, le professeur Piazza, 54 ans, recevait le Grand Prix Inserm 2015 « pour l’ensemble de ses recherches sur les mécanismes physiopathologiques des maladies psychiatriques ». Le 24 novembre, l’Académie des sciences l’honorait du prix Lamonica de neurologie.

C’est dans la voie des addictions, et des raisons pour lesquelles certains y sont plus vulnérables que d’autres, qu’il s’est illustré. Une voie jalonnée, depuis 1989, par six publications dans la revue Science, et quelques autres dans PNAS et Nature Neuroscience.« Le docteur Piazza est, au plan international, un des experts les plus reconnus de la recherche en addictologie, estime le professeur Yavin Shaham, responsable des neurosciences comportementales du National Institute on Drug Abuse (NIDA), à Baltimore (Etats-Unis). Ses nombreux travaux publiés, issus de l’étude de modèles animaux, ont eu un impact notable sur l’orientation des recherches de ce domaine. » Travaux que Pier Vincenzo Piazza résume...

Structural-functional connectivity deficits of neocortical circuits in the Fmr1−/y mouse model of autism
Matthias G. Haberl , Valerio Zerbi, Andor Veltien, Melanie Ginger, Arend Heerschap and Andreas Frick

Abstract :
Fragile X syndrome (FXS), the most common inherited form of intellectual disability disorder and a frequent cause of autism spectrum disorder (ASD), is characterized by a high prevalence of sensory symptoms. Perturbations in the anatomical connectivity of neocortical circuits resulting in their functional defects have been hypothesized to contribute to the underlying etiology of these disorders. We tested this idea by probing alterations in the functional and structural connectivity of both local and long-ranging neocortical circuits in the Fmr1−/y mouse model of FXS. To achieve this, we combined in vivo ultrahigh-field diffusion tensor magnetic resonance imaging (MRI), functional MRI, and viral tracing approaches in adult mice. Our results show an anatomical hyperconnectivity phenotype for the primary visual cortex (V1), but a disproportional low connectivity of V1 with other neocortical regions. These structural data are supported by defects in the structural integrity of the subcortical white matter in the anterior and posterior forebrain. These anatomical alterations might contribute to the observed functional decoupling across neocortical regions. We therefore identify FXS as a “connectopathy,” providing a translational model for understanding sensory processing defects and functional decoupling of neocortical areas in FXS and ASD.

Connexions défaillantes à travers le cerveau, en cause dans certains troubles de l’autisme