Dynamique et plasticité dans les réseaux de neurones à impulsions. Etude du couplage temporel réseau/agent/environnement

Dans ce travail, une approche de "vie artificielle" est utilisée pour étudier le support neural des comportements. Un comportement est issu d\u27une bonne adéquation entre le système de contrôle, les capacités sensori-motrices de l\u27agent et de l\u27environnement. Dans un paradigme dynamique, un comportement est ainsi un attracteur dans l\u27espace perception/action - composé de la dynamique interne du contrôleur et de celle obtenue par l\u27évolution de l\u27agent. La dynamique neurale est à l\u27origine de la dynamique interne. L\u27apprentissage de comportement revient donc à coupler ces deux dynamiques. Nous introduisons, dans un premier temps, une étude détaillée de la dynamique nerveuse dans le cas de réseaux de neurones à impulsions. En mode spontané (c\u27est-à-dire sans entrées), ces réseaux opèrent de manière non triviale. Selon les paramètres de la distribution de poids synaptiques, nous sommes en mesure d\u27estimer complètement l\u27activité de décharge. On montre l\u27existence d\u27une bifurcation pour le paramètre de couplage : la variance de la distribution. Nous montrons aussi que ce facteur de couplage mesure le charactère chaotique du fonctionnement du réseau. Pour apprendre des comportement, nous utilisons un algorithme biologiquement plausible la Spike-Time Dependent Plasticity qui permet de coupler la dynamique neurale. Nous montrons en dynamique spontanée l\u27influence des paramètres d\u27apprentissage sur le fonctionnement du réseau. Nous montrons que la STDP permet de rester dans un régime "au bord du chaos". Dans le but de valider cette approche, nous utilisons le réseau pour controler un robot qui doit apprendre à éviter les obstacles en servant uniquement du flot visuel

Enhanced Stimulus Encoding Capabilities with Spectral Selectivity in Inhibitory Circuits by STDP

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Membrane microdomains emergence through non-homogeneous diffusion.

International audienceBACKGROUND: In the classical view, cell membrane proteins undergo isotropic random motion, that is a 2D Brownian diffusion that should result in an homogeneous distribution of concentration. It is, however, far from the reality: Membrane proteins can assemble into so-called microdomains (sometimes called lipid rafts) which also display a specific lipid composition. We propose a simple mechanism that is able to explain the colocalization of protein and lipid rafts. RESULTS: Using very simple mathematical models and particle simulations, we show that a variation of membrane viscosity directly leads to variation of the local concentration of diffusive particles. Since specific lipid phases in the membrane can account for diffusion variation, we show that, in such a situation, the freely diffusing proteins (or any other component) still undergo a Brownian motion but concentrate in areas of lower diffusion. The amount of this so-called overconcentration at equilibrium issimply related to the ratio of diffusion coefficients between zones of high and low diffusion. Expanding the model to include particle interaction, we show that inhomogeneous diffusion can impact particles clusterization as well. The clusters of particles were more numerous and appear for a lower value of interaction strength in the zones of low diffusion compared to zones of high diffusion. CONCLUSION: Provided we assume stable viscosity heterogeneity in the membrane, our model propose a simple mechanism to explain particle concentration heterogeneity. It has also a non-trivial impact on density of particles when interaction is added. This could potentially have an impact on membrane chemical reactions and oligomerization

Modélisation cellulaire pour l'émergence de structures multiprotéiques auto-organisées

National audienceSystems biology and cell simulation started together and maintain a controvertible relationship within the scope of global approaches and emergence-driven approaches. Here, we present a multi-agent based model for cell simulation. We describe the whole model creation process, from its scientific project perspective to implementation considerations. The agents interactions model will be particularly detailed. Finally, preliminary results showing self-organised structures will be presented to demonstrate the interest of this approach.La biologie des systèmes et la simulation cellulaire sont nées conjointement et entretiennent des relations ambiguës entre approches globalisantes et approches émergentistes. Nous présentons ici une démarche émergentiste de la modélisation cellulaire, basée sur une simulation multiagent. Nous décrivons l'ensemble du processus de création du modèle, depuis le projet scientifique jusqu'aux méthodes d'implémentation, en insistant particulièrement sur le modèle d'interactions entre agents qui est la base de notre simulation. Enfin, des résultats préliminaires montrant l'émergence de structures organisées sont présentés pour illustrer l'intérêt de l'approche proposée

Housing conditions and sacrifice protocol affect neural activity and vocal behavior in a songbird species, the zebra finch (Taeniopygia guttata).

International audienceIndividual cages represent a widely used housing condition in laboratories. This isolation represents an impoverished physical and social environment in gregarious animals. It prevents animals from socializing, even when auditory and visual contact is maintained. Zebra finches are colonial songbirds that are widely used as laboratory animals for the study of vocal communication from brain to behavior. In this study, we investigated the effect of single housing on the vocal behavior and the brain activity of male zebra finches (Taeniopygia guttata): male birds housed in individual cages were compared to freely interacting male birds housed as a social group in a communal cage. We focused on the activity of septo-hypothalamic regions of the "social behavior network" (SBN), a set of limbic regions involved in several social behaviors in vertebrates. The activity of four structures of the SBN (BSTm, medial bed nucleus of the stria terminalis; POM, medial preoptic area; lateral septum; ventromedial hypothalamus) and one associated region (paraventricular nucleus of the hypothalamus) was assessed using immunoreactive nuclei density of the immediate early gene Zenk (egr-1). We further assessed the identity of active cell populations by labeling vasotocin (VT). Brain activity was related to behavioral activities of birds like physical and vocal interactions. We showed that individual housing modifies vocal exchanges between birds compared to communal housing. This is of particular importance in the zebra finch, a model species for the study of vocal communication. In addition, a protocol that daily removes one or two birds from the group affects differently male zebra finches depending of their housing conditions: while communally-housed males changed their vocal output, brains of individually housed males show increased Zenk labeling in non-VT cells of the BSTm and enhanced correlation of Zenk-revealed activity between the studied structures. These results show that housing conditions must gain some attention in behavioral neuroscience protocols

Intestinal alteration of α-gustducin and sweet taste signaling pathway in metabolic diseases is partly rescued after weight loss and diabetes remission Running Head: Intestinal α-gustducin in metabolic diseases

International audienceCarbohydrates and sweeteners are detected by the sweet taste receptor in enteroendocrine cells (EEC). This receptor is coupled to the gustducin G-protein, which α-subunit is encoded by GNAT3 gene. In intestine, the activation of sweet taste receptor triggers a signaling pathway leading to GLP-1 secretion, an incretin hormone. In metabolic diseases GLP-1 concentration and incretin effect are reduced while partly restored after Roux-en-Y gastric bypass (RYGB). We wondered if the decreased GLP-1 secretion in metabolic diseases is caused by an intestinal defect in sweet taste transduction pathway. In our RNA-sequencing of EEC GNAT3 expression is decreased in patients with obesity and type 2 diabetes compared to normoglycemic obese patients. This prompted us to explore sweet taste signaling pathway in mice with metabolic deteriorations. During obesity onset in mice Gnat3 expression was downregulated in EEC. After metabolic improvement with entero-gastro anastomosis surgery in mice (a surrogate of the RYGB in humans), the expression of Gnat3 increased in the new alimentary tract and glucose-induced GLP-1 secretion was improved. In order to evaluate if high-fat diet-induced dysbiotic intestinal microbiota could explain the changes in the expression of sweet taste α-subunit G protein, we performed a fecal microbiota transfer in mice. However, we could not conclude if dysbiotic microbiota impacted or not intestinal Gnat3 expression. Our data highlight that metabolic disorders were associated with altered gene expression of sweet taste signaling in intestine. This could contribute to impaired GLP-1 secretion that is partly rescued after metabolic improvement

Type 2 diabetes is associated with impaired jejunal enteroendocrine GLP-1 cell lineage in human obesity

International audienceObjectives: Altered enteroendocrine cell (EEC) function in obesity and type 2 diabetes is not fully understood. Understanding the transcriptional program that controls EEC differentiation is important because some EEC types harbor significant therapeutic potential for type 2 diabetes.Methods: EEC isolation from jejunum of obese individuals with (ObD) or without (Ob) type 2 diabetes was obtained with a new method of cell sorting. EEC transcriptional profiles were established by RNA-sequencing in a first group of 14 Ob and 13 ObD individuals. EEC lineage and densities were studied in the jejunum of a second independent group of 37 Ob, 21 ObD and 22 non obese (NOb) individuals.Results: The RNA seq analysis revealed a distinctive transcriptomic signature and a decreased differentiation program in isolated EEC from ObD compared to Ob individuals. In the second independent group of ObD, Ob and NOb individuals a decreased GLP-1 cell lineage and GLP-1 maturation from proglucagon, were observed in ObD compared to Ob individuals. Furthermore, jejunal density of GLP-1-positive cells was significantly reduced in ObD compared to Ob individuals.Conclusions: These results highlight that the transcriptomic signature of EEC discriminate obese subjects according to their diabetic status. Furthermore, type 2 diabetes is associated with reduced GLP-1 cell differentiation and proglucagon maturation leading to low GLP-1-cell density in human obesity. These mechanisms could account for the decrease plasma GLP-1 observed in metabolic diseases