Séminaires des laboratoires

16/10/2017 - LNC - Rochelle Ackerley (Laboratoire de Neurosciences Intégratives et Adaptatives, Marseille)

Rochelle Ackerley (Laboratoire de Neurosciences Intégratives et Adaptatives, Marseille)

Stimulating single tactile afferents in humans : sensations felt and cortical responses generated

Our touch system presents a complex network of afferents, where a multitude of sensations can be felt, from more simple facets like vibration to blended percepts such as wetness. The technique of microneurography permits recordings from single human afferents, via the insertion of an electrode into a peripheral nerve. Mechanical stimuli can be applied to the skin and the responses from tactile afferents can be recorded. This can be taken one step further, by recording from a single afferent and then stimulating the same one, by applying a small electrical current down the electrode. In essence, it is possible to record signals from one mechanoreceptive afferent, then artificially stimulate it to produce a perceptual tactile experience, where questions can be asked about the illusory sensation generated. I combine this approach with high resolution brain imaging, to understand the precise somatosensory circuits that encode such fundamental touch. These findings can be applied in the domain of emulating cutaneous signals, such as recovering touch in amputees. The implementation of somatosensory feedback for missing body parts represents an immense step forward in the development and use of prostheses.

16/10/2017 à 13:30

13/10/2017 - LNC - Séminaire Emmanuel Barbeau

11 heures - LPC, Salle des Voûtes, Campus St Charles - 13003 Marseille

Emmanuel Barbeau
Centre de Recherche Cerveau et Cognition, UMR5549, Toulouse, France

Familiarity and recollection: revisiting dogmas

We recognize everyday dozens of objects and faces. Actually this ability is so efficient that we do not even pay any attention to it. However, it has been shown that we can rapidly store thousands of new pictures and sometimes for a very long time without rehearsal in the meantime. Phenomenologically two processes are supposed to participate to recognition memory, one fast and acontextual called familiarity, the other slower and associated with the context in which the stimulus was encountered called recollection. Although there is agreement on the core network of brain regions involved in recollection, surprisingly little is known about familiarity, quite probably because the psychological and physiological signals associated with familiarity are fast, but also much weaker, than those associated with recollection. In fact, it is not even clear if familiarity is a single process as often presented. In this talk, I will review recent studies in which we used a combination of new paradigms, neuropsychological and intracerebral electrophysiological studies to identify the network of brain regions involved in familiarity.

06/10/2017 - LPC - Séminaire George Michael

 

11 heures - LPC, Salle des Voûtes, Campus St Charles - 13003 Marseille

George Michael
Université Lumière, Lyon 2

29/09/2017 - LPC - Séminaire Corentin Gonthier

Séminaire Corentin Gonthier

11 heures - LPC, Salle des Voûtes, Campus St Charles - 13003 Marseille

Corentin Gonthier
MCF en psychologie différentielle et statistiques
LPE - CRPCC Université Rennes 2

Un contrôle cognitif sans fonctions exécutives : la variabilité selon le modèle à deux mécanismes de contrôle (DMC)

L'aptitude des individus à réguler leur comportement est souvent étudiée sous l'angle des fonctions exécutives : des fonctions élémentaires comme l'inhibition ou la flexibilité. Mais une autre approche consiste à définir le contrôle cognitif comme une aptitude relativement unitaire, ce qui ouvre la voie à des recherches portant sur la façon dont ce contrôle est mis en place. Le modèle à deux mécanismes de contrôle (DMC : Braver et al., 2007) propose par exemple que le contrôle cognitif peut se faire de façon proactive ou de façon réactive.
Je présenterai cette approche originale du contrôle cognitif et une série de travaux portant sur la mesure des mécanismes de contrôle proactif et réactif, la possibilité d'induire les participants à utiliser l'un des deux mécanismes, et leur lien avec la capacité en mémoire de travail.

26/09/2017 - LNIA - “Involvement of the thalamic nucleus réunies in the hippocampo-cortical coupling”

Dr. Pascale Quilichini, Institut de Neurosciences des Systèmes, PhysioNet Team, INSERM U1106

“Involvement of the thalamic nucleus réunies in the hippocampo-cortical coupling”
mardi 26 septembre 2017, de 11h à 12h (invité par JL. Blanc).

15/09/2017 - LPC - Séminaire Zoltan Dienes

 

11 heures - LPC, Salle des Voûtes, Campus St Charles - 13003 Marseille

Zoltan Dienes
Professor of Psychology
School of Psychology
University of Sussex

07/07/2017 - LPC - Séminaire Susana Chung

11 heures - LPC, Salle des Voûtes - campus St Charles - 13003 Marseille

Susana Chung
Berkeley University of California

03/07/2017 - LNC - Nicolas Mallet (Institut des maladies neurodégénératives, Bordeaux)

 

Optogenetic dissection of circuit mechanism underlying beta-oscillation expression in Parkinsonism

The basal-ganglia (BG) form a complex loop with the cortex and the thalamus that is involved in action selection and movement control. Synchronized oscillatory activities in BG neuronal circuits have been proposed to play a key role in coordinating information flow within this neuronal network. If synchronized oscillatory activities are important for normal motor function, their dysregulation in space and time could be truly pathological. Indeed, in Parkinson’s disease (PD), many studies have reported an abnormal increase in the expression level of neuronal oscillations contained in the beta (β) frequency range (15-30 Hz). These abnormal β oscillations have been proposed to be responsible for two motor symptoms of PD : akinesia and bradykinesia. However, which neuronal circuits generate these abnormal β oscillations that propagate through the entire BG loop is not known. The subthalamic nucleus (STN) is a key nucleus in BG that receives converging inputs from the motor cortex (mCx) and the external globus pallidus (GP). It has been proposed that the reciprocally connected STN-GP microcircuit could act as a pacemaker that generates pathological oscillatory activity in BG but it is difficult to rule out the influence of mCx in this generation mechanism. Here, we used a rat model of PD combined with in vivo electrophysiological recordings and optogenetic manipulations to directly dissect how selective control of mCx, STN and GP causally influence BG network dynamic at beta frequencies. Our data both challenge the implication of mCx and STN in the generation mechanisms of abnormal β-oscillations but highlight the central role of GP that is necessary and sufficient for the maintenance of synchronized β activities in dopamine-depleted state.

 

12/06/217 - LNC - Bruno Lebrun (Laboratoire de Physiologie et Physiopathologie du Système Nerveux Somato-Moteur et Neurovégétatif))

enir (upcoming seminars)

Bruno Lebrun (Laboratoire de Physiologie et Physiopathologie du Système Nerveux Somato-Moteur et Neurovégétatif))

Les cellules gliales : des acteurs de poids dans le contrôle de l’homéostasie énergétique

Alors que depuis deux décennies, les efforts se concentrent sur l’identification des réseaux neuronaux de l’hypothalamus et du complexe vagal dorsal (CVD) impliqués dans la régulation homéostatique de la balance énergétique, nous avons choisi de tester l’hypothèse de l’implication des cellules gliales dans ces régulations. Dans ce contexte, nous nous intéressons particulièrement aux endozépines. Les endozépines sont connues pour induire un effet anorexigène, indépendamment de leur action sur les récepteurs des benzodiazépines. Nous avons montré que les endozépines sont exprimées par plusieurs populations gliales dans l’hypothalamus et le CVD, à des niveaux dépendant du statut nutritionnel. De façon intéressante, nous avons observé, chez des souris rendues résistantes à la leptine par une nourriture enrichie en graisses, qu’un traitement central par les endozépines permet de normaliser la sensibilité à la leptine et de supprimer l’hyperphagie et le surpoids de ces souris. Cette action impliquerait une augmentation du transport de la leptine vers le parenchyme cérébral et ceci via une sous population gliale particulière les tanycytes. Parallèlement, nous recherchons par quel(s) mécanisme(s) les cellules gliales de l’hypothalamus et du CVD peuvent libérer des substances susceptibles de modifier la balance énergétique. Les connexines Cx43 exprimées par les cellules gliales et formant non seulement des jonctions communicantes mais également des hémi-canaux connus pour permettre l’émission de gliotransmetteurs sont des candidates potentielles. Le niveau d’expression de Cx43 dans l’hypothalamus et le CVD est fonction du statut nutritionnel. L’administration centrale d’un agent pharmacologique empêchant sélectivement l’ouverture des hémi-canaux de Cx43 entraîne un fort effet anorexigène et recrute les neurocircuiteries anorexigènes de l’hypothalamus et du CVD. Ces résultats suggèrent que les cellules gliales peuvent également émettrent de façon tonique des gliotransmetteurs orexigènes via les hémi-canaux Cx43. A la lumière de ces résultats, nous pensons que le compartiment glial doit être pris en compte dans l’étude du contrôle de l’homéostasie énergétique, et nous développons actuellement plusieurs modèles génétiques pour conforter nos observations. A terme, nous pensons qu’une meilleure compréhension du compartiment glial de l’hypothalamus et de CVD est susceptible de fournir des pistes thérapeutiques originales pour lutter contre les dérèglements de la balance énergétique.

 

09/06/2017 - LNC - Neil Schwartz (Univ California, San Francisco)

Neil Schwartz (Univ California, San Francisco)

Cortico-striatal regulation of conflicting behavioral drives​

I am interested in experience- and pathological-associated regulation of motivated behavior. In my talk, I’ll describe 2 projects in which we investigated how experience-dependent and chronic pain-associated changes in cortico-striatal circuits regulate approach-avoidance choice and motivation to work for a reward.

 

02/06/2017 - LPC - Séminaire Aurélie Calabrèse

 

11 heures - LPC, Salle des Voûtes, Campus St Charles - 13003 Marseille

Aurélie Calabrèse
Laboratoire de Psychologie Cognitive
CNRS & AMU

Understanding the reading deficits of individuals with central vision loss to help restore their reading abilities.

Age-related macular degeneration (AMD) accounts for 8.7% of all blindness worldwide and is the most common cause of blindness in developed countries. Older adults suffering from AMD often lose the ability to use central vision after developing a central scotoma. Despite advances in the treatment of wet AMD, central vision cannot be restored and difficulty with reading is often the primary complaint of AMD patients, who have to use their peripheral vision for reading. The number of Europeans with AMD, and who struggle with reading, is expected to reach 60 million by 2030. When eye disorders limit people’s access to printed text, the issue is vision disability, not literacy, but the individual consequences may be just as severe.

The focus of this talk will be to present some of the latest progress made to understand (and therefore overcome) the underlying factors of the reading deficits following central vision loss (CVL). Questions that will be covered include: what sensory, cognitive and oculo-motor factors can explain slow reading speed with CVL? Can reading performance be improved through training and what are the cortical sites involved in this improvement? How to optimize reading aids and reading diagnostic tools?

24/04/2017 - LNC - Christian Ruff (Laboratory for Social and Neural Systems Research, Université de Zurich)

 Christian Ruff (Laboratory for Social and Neural Systems Research, Université de Zurich)  24/04/2017 à 13:30

03/04/2017 - LNC - Randi Starrfelt (University of Copenhague)

 Randi Starrfelt (University of Copenhague)  03/04/2017 à 13:30

27/03/2017 - LNC - Giulio Casali (UCL, London)

 Giulio Casali (UCL, London)  27/03/2017 à 13:30

10/03/2017 - LPC - Steve Fleming

Vendredi 10 mars 2017 - LPC
Steve Fleming
Wellcome Trust Centre for Neuroimaging
University College London

30/01/2017 - LNC - Laure Verret (CNRS/Université Paul Sabatier, Toulouse)

Laure Verret (CNRS/Université Paul Sabatier, Toulouse)

Social Memory Impairments and Area CA2 Modifications in a Mouse Model of Alzheimer’s Disease

Among the cognitive impairments observed in Alzheimer’s disease (AD) patients, one of the most excruciating is their inability to recognize or remember other people. Distressingly, social memory and recognition have been barely investigated in AD mouse models, and little is known about the neural substrates of social memory impairments in AD. Very recently, it has been demonstrated that inactivation of area CA2 pyramidal neurons induces specific social memory impairments (Hitti & Siegelbaum 2014), and this hippocampal structure is now considered as a critical hub for sociocognitive memory processing (Chevaleyre & Piskorowski 2016). Thus, we hypothesized that social memory impairments in AD mouse models could be mediated by area CA2 dysfunction. We observed anatomical modifications in the area CA2 of AD mice, which are inducing decreased inhibitory control of CA2 pyramidal cells, and are associated with social recognition and social memory impairments. We are now exploring whether there is a causal link between these anatomical alterations in area CA2 and social memory deficits in the context of AD.
 

30/01/2017 à 13:30