Dean BUONOMANO, professor of psychology and neurobiology at the University of California, Los Angeles (UCLA)

The ability to tell time, represent and encode temporal information, and use past experiences to predict the future, are among the most fundamental computations the brain performs. But how do networks of neurons tell time and encode temporal information in a flexible manner? Precisely because of the importance of time, we argue that most neural circuits are capable of temporal computations. But in contrast to the clocks on our wrists that rely on the same mechanism to tell time across a wide range of scales, the brain engages many different mechanisms and circuits to tell time. We and others have proposed that on the scale of seconds timing relies on neural population clocks: time-varying patterns of neural activity that emerge from the dynamics of recurrent neural circuits. More generally, we propose that such dynamic regimes represent a fundamental computational strategy in the brain.

Entrée gratuite, mais inscription obligatoire sur https://www.eventbrite.com/e/billets-visites-du-centre-de-recherche-en-biomedecine-de-strasbourg-853544423347?aff=oddtdtcreator

PROGRAMMATION

10h : Ouverture des portes

Conférences grand public

Durée : 20 min de présentation, 10 min pour répondre à vos questions – À partir de 7 ans

• 10h30 : « Trouble de l’usage d’opiacés et marqueurs biopsychosociaux : à propos de deux projets », Pr. Laurence LALANNE
• 11h30 : « Actualités sur le Sclérose Latérale Amyotrophique ou Maladie de Charcot », Dr. Marie-Céline FLEURY
• 14h30 : « Le cerveau, un organe aux frontières bien gardées : exemple de la barrière hémato-encéphalique », Dr. Guillaume BECKER

Visites de nos locaux

Durée : 30min par visite – À partir de 7 ans

• Visite guidée de la plateforme d’imagerie
• Visite guidée d’un laboratoire de recherche

Ateliers ludiques autour de la science

Durée : 5-10min par atelier – À partir de 7 ans

• Hypothèse anatomo-fonctionnelle : découvrez comment est organisé le cerveau et comment chaque région se spécialise dans une fonction
• Les neurones communiquent : apprenez comment l’information est transmise dans les différentes zones du cerveau, et participez à un jeu où votre rapidité sera mise à l’épreuve !
• Colore ton neurone : à travers la coloration d’une lame, découvrez comment marquer et observer les neurones
• Développement cérébral : observez l’évolution du cerveau entre différentes espèces animales
• Défie ton cerveau ! Défiez votre cerveau avec des jeux de mémoire ou logique et des illusions d’optique !

Stands associatifs

• Association pour la Recherche sur la Sclérose Latérale Amyotrophique (ARSLA)
• Épilepsie France (10h-10h30 uniquement)
• Association Huntington France (AHF)

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease of the adult motor system, for which effective treatments remain elusive. Mutations leading to the mislocalization of FUS, an essential RNA-binding protein, have been linked to the most severe form of ALS. Despite intense research efforts, the cascade of pathological events triggering the progressive degeneration of motor neurons remains incompletely understood. Our prior investigations revealed significant lipid metabolism alterations in the spinal cord of a FUS mouse model, as well as in motor neurons derived from ALS patients induced pluripotent stem cells (iPSCs). Recent evidence suggests that dysfunctional glial cells, including oligodendrocytes, contribute to neurodegeneration in FUS-linked ALS through non-cell autonomous mechanisms. In our latest research, we investigated the impact of FUS mutations in oligodendrocyte progenitor cells (OPCs) derived from human iPSCs. Confirming the cytoplasmic mislocalization of FUS in OPCs, we uncovered significant alterations in lipid metabolism, accompanied by transcriptomic alterations related to myelin formation. Additionally, we observed mitochondria-associated ER membrane abnormalities, ER stress, and mitochondrial dysfunctions. These recent findings emphasize the pathological role of FUS in oligodendrocytes, shedding light on the intricate cellular mechanisms contributing to FUS-linked ALS pathology.

Un contrat IE de 2 ans (débutant janvier 2024) est ouvert à l’INCI UPR3212 pour mener un projet de neuroanatomie humaine (histologie, immunohistochimie, RNAscope).
Pour candidater et pour plus d’information, merci de contacter : Michel Barrot (mbarrot@inci-cnrs.unistra.fr) à l’INCI.

Bio: Philipp Sterzer is a psychiatrist, neurologist and neuroscientist who trained in Frankfurt am Main, London and Berlin and held a professorship for psychiatry and computational neuroscience at Charité Berlin from 2011 to 2022. Recently, he was appointed Professor of Translational Psychiatry at University of Basel, Switzerland. His work focuses on the investigation of predictive neural processes in perception and their alterations in psychotic disorders using functional neuroimaging and computational modeling among other methods. Along with numerous articles in scientific journals and textbooks, he recently published “Die Illusion der Vernunft”, a popular science book on delusions and other irrational beliefs.

This event will feature the latest scientific and clinical developments in pain assessment and treatment, mood disorders and comorbidities, pain evaluation and technologies (programme below).

The number of participants will be limited to 70, therefore registration is MANDATORY.
Please REGISTER HERE before 25.05.2023. 

Location
Doctoral College
Amphitheatre – Ground Floor
46 boulevard de la Victoire – 67100 Strasbourg

How different complex features of the dynamics emerge from a given structural connectivity (SC) is of great interest for our understanding of brain function, in health and disease. Among the complex dynamical features that are commonly described, the continuously evolving correlation patterns of the brain (Functional Connectivity Dynamics, FCD) has been extensively characterized and described as a marker for aging and psychiatric disorders. More recently, the existence of high-order interdependencies of either synergistic or redundant types has also been shown to change with aging, with brain activity from older healthy subjects showing more redundancy. To understand how different topological features of the structural connectome can be related to these features of the functional connectivity, we built a set of 240-node structural connectomes with varying degrees of integration and segregation, assessed with metrics from network analysis. These connectomes included artificial networks such as Watts-Strogatz or modular networks, and empirical human connectomes that were perturbed to manipulate their integration and segregation measures. The set of over 40 SCs spanned a broad range of the small-world coefficient omega, sweeping from lattice-like to small-world to random-like networks. Then the SCs were used to simulate neural activity using a Wilson-Cowan model modified with homeostatic inhibitory plasticity, to ensure an oscillatory regime over a wide range of the global connectivity parameter G. Then, the simulated activity was assessed for the FCD, using the variance of the FCD matrix as an index for dynamical richness, and for the emergence of synergistic interdependencies, by randomly sampling groups of 3, 4, or 5 nodes. The nature of the high-order dependencies was assessed using the O-information metric, that is negative for systems dominated by synergy and positive for those with more redundancy. In all the networks, the higher variance of FCD and the most synergistic n-plets were found at an intermediate value of G, were the metastability is also high and the network synchrony is moderate. When looking at the structural features, the networks that maximized both complex dynamical features were those having a positive omega index but close to zero. This indicates networks of the small-world type, which have a balance between their integration and segregation metrics. Our results are in agreement with what has been observed in the brain SC and its dynamics as the brain ages.

The Scheiffele group uses an in vivo cell biology approach to uncover mechanisms of neuronal network formation in health and disease. They are seeking to understand molecular mechanisms of synapses formation, developmental remodeling, and plasticity. They apply a broad range of molecular, anatomical, imaging, electrophysiological, and behavioral assessments in rodents. A particular focus is on mRNA alternative splicing and translation, and its dysregulation in autism spectrum disorders. Based on the insights in developmental studies, the Scheiffele lab is developing therapeutic strategies using small molecules and splicing therapeutics for genetically-defined neurodevelopmental conditions.

See also: https://www.biozentrum.unibas.ch/research/research-groups/research-groups-a-z/overview/unit/research-group-peter-scheiffele

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Comité d'Animation et de Communication  Scientifique de l'INCI
Amandine Bery, Caroline George, Jennifer Kaufling, Marie-Pierre Laran-Chich, Hervé Cadiou, Stéphane Gasman, Yannick Goumon & Antoine Valéra