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X-WR-CALNAME:Bordeaux Neurocampus
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X-WR-CALDESC:Events for Bordeaux Neurocampus
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DTSTART:20240331T010000
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DTSTART;TZID=Europe/Paris:20241213T100000
DTEND;TZID=Europe/Paris:20241213T100000
DTSTAMP:20260422T094516
CREATED:20241024T094920Z
LAST-MODIFIED:20241212T114322Z
UID:176910-1734084000-1734084000@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Juan Estaun Panzano
DESCRIPTION:Venue : Centre Broca Nouvelle-Aquitaine \n \nDefense in english \n\nJuan Estaun Panzano\nIMN\nThesis director : Erwan Bézard \nTitle\nExtracellular space in neurodegenerative disorders \nAbstract\nThe extracellular space (ECS)\, comprising the narrow compartment between the cells filled with interstitial fluid and the extracellular matrix (ECM) it is key for communication and transport between brain cells and is vital for maintaining brain homeostasis. In this work\, we try to shed some light on the potential alterations of the ECS in the proteinopathies context\, particularly synucleinopathy and amyloid pathology. These protein accumulations are known to disrupt normal brain functions\, but their impact on the brain’s ECS\, which plays a critical role in molecular/protein diffusion and waste clearance\, has not been thoroughly examined. \nIn the introduction\, I present an overview of amyloid and α-synuclein pathology. Later\, ECS and its components will be introduced\, focusing on the extracellular matrix and diffusion processes. Furthermore\, the glymphatic system\, a proposed waste-clearance mechanism linked to the ECS\, is discussed. Understanding these mechanisms is crucial for interpreting how the ECS is altered in proteinopathies and its repercussions. Additionally\, the study reviews current techniques used to investigate the ECS\, including traditional methods\, advanced imaging\, and single-particle tracking techniques. \nI then present the structural and rheological changes in the ECS in two different models of proteinopathies\, focusing on the altered diffusion properties within this space and its implications for disease pathology. A variety of advanced techniques were employed to address these questions.  In the first sub-project\, we report ECS diffusivity changes in the striatum of a mouse synucleinopathy model. Using single-walled carbon nanotube (SWCNTs) tracking in the ECS\, the study demonstrates that intracellular α-synuclein assemblies can significantly alter nanoscale diffusion in the striatal ECS. \nWe repeat the same approach in an amyloid mouse model (APP/PS1)\, with special focus on diffusion alterations around amyloid plaques and its fine relationship with matrix disruptions. We employed a complementary set of nanoscopic imaging techniques to investigate the ECS alterations: Two-photon shadow imaging in vivo and ex vivo\, revealed cortical amyloid as a dense ring of cells and a central core. Quantum dot SPT tracking unraveled the core of the plaque is not easily penetrable by ab-sized molecules. Furthermore\, we report ECS rheological parameters are heterogeneous in and around plaques\, with an increased diffusivity in the amyloid animal and low nanoparticle density in the core. Using SWCNTs\, we confirmed these altered local diffusion properties in the cortex of AD mice\, with an overall higher local diffusivity in APP/PS1 cortex. We found an altered ECM\, notably disrupted within the amyloid plaque but not only\, providing a rationale for the altered rheological dynamics in AD brain tissue and shedding new light on strategies to develop effective Aβ plaques-penetrating therapies. \nOverall\, the findings presented in this work contribute to a deeper understanding of the ECS’s role and changes in neurodegenerative diseases. The results suggest that altered diffusion of the brain ECS are a relatively common phenomenon. Future modelling studies of disease expansion or therapeutics design should considerthese changes. \nKey words\nExtracellular space\, Extracellular diffusion\, Single-particle tracking\, α-synuclein\, Parkinson’s disease\, amyloid beta\, amyloid plaques\, Alzheimer’s disease\, Extracellular matrix\, Quantum Dots\, Single-wall carbon Nanotubes \nPublications \n\nEstaun-Panzano\, J.\, Arotcarena\, M. L.\, & Bezard\, E. (2023). Monitoring α-synuclein aggregation. Neurobiology of disease\, 176\, 105966. \nJury\n\nDr. José A. Obeso\, Professor of Neurology\, CEU-San Pablo University\, President\nDr. Rosario Moratalla\, Research Professor\, Cajal Institute\, External reviewer\nDr. Federico Nicolás Soria\, Ikerbasque Research Fellow\, Basque Center for Neuroscience\, External reviewer\nDr. Erwan Bezard\, Directeur de Recherche\, INSERM\, Thesis director\n\n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-juan-estaun-panzano/
CATEGORIES:IMN,Thesis
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241213T100000
DTEND;TZID=Europe/Paris:20241213T113000
DTSTAMP:20260422T094516
CREATED:20241209T062634Z
LAST-MODIFIED:20241209T062634Z
UID:178784-1734084000-1734089400@www.bordeaux-neurocampus.fr
SUMMARY:Mini-symposium: Brain states\, sensory processing and transformation into action in neurotypical and autistic conditions
DESCRIPTION:Venue: BBS \nOrganized by Andreas Frick and Théo Gauvrit \n\nSpeakers \nIan Duguid\, University of Edinburgh (UK) \nBrice Bathellier\, Institut Pasteur (France) \nElizabeth Milne\, The University of Sheffield (UK) \nElizabeth Milne\nResting State EEG biomarkers for autism: sparse findings from a large sample \nSubstantial research time has been dedicated to the search for an EEG-based biomarker for autism. However\, despite intensive effort\, no single biomarker nor common understanding about the way(s) in which neural dynamics may differ between autistic and neurotypical people has been identified. \nIn this talk\, I will present the results of a large-scale secondary data analysis project where we compared eyes-open resting state EEG dynamics between autistic and neurotypical people in a sample of 776 participants (421 autistic\, 355 neurotypical) and in a follow-up study where we analysed both eyes-open and eyes-closed resting state data in a sample of 300 participants (126 autistic and 355 neurotypical). \nWe took an extremely exploratory approach\, extracting 726 variables from each participant reflecting absolute and relative power across six frequency bands; 1/f aperiodic activity; multiscale entropy\, phase-amplitude coupling\, and intersite phase coherence. After computing effect size and split-half reliability coefficients\, we found very few variables that reliably differed between the autistic and neurotypical samples\, although we noted that reliable group differences were more likely to be observed in data acquired during eyes-closed resting than eyes-open resting state. Group differences\, where they occurred\, were found primarily in variables that reflected relative power and hemispheric power asymmetry\, particularly in the lower frequency bands (delta\, alpha)\, and multi-scale entropy over frontal regions. \nThese data speak strongly to the heterogeneity and inter-individual variability of the autism profile and pose a substantial challenge to projects that aim to identify a single biomarker that reflects the diagnostic label of autism. \n  \nBrice Bathellier\nA spatial code for temporal information is necessary for efficient sensory learning \nThe temporal structure of sensory inputs contains essential information for their interpretation. Sensory cortex represents these temporal cues through two codes: the temporal sequences of neuronal activity and the spatial patterns of neuronal firing rate. However\, it is unknown which of these coexisting codes causally drives sensory decisions. To separate their contributions\, we generated in the mouse auditory cortex optogenetically-driven activity patterns differing exclusively along their temporal or spatial dimensions. Mice could rapidly learn to behaviorally discriminate spatial but not temporal patterns. Moreover\, large-scale neuronal recordings across the auditory system revealed that the auditory cortex is the first region in which spatial patterns efficiently represent temporal cues on the time scale of several hundred milliseconds. This feature is shared by the deep layers of neural networks categorizing time-varying sounds. Therefore\, the emergence of a spatial code for temporal sensory cues is a necessary condition to efficiently associate temporally structured stimuli with decisions. \n  \nIan Duguid\nCorticospinal neurons in efficient response control \nThe ability to execute appropriate actions in response to salient environmental cues is termed response control. This requires brain-wide sensory-to-action transformations\, involving sensory perception\, motor planning\, and ultimately movement execution\, the latter being driven in part by a subset of motor cortical projection neurons with direct access to the spinal cord. These corticospinal neurons (CSNs) provide time-varying spinal cord input to orchestrate complex muscle synergies necessary for executing skilled movements and disrupting their output leads to loss of limb function\, impaired reach precision\, and hand discoordination. While CSN activation has been associated with movement execution and kinematic parameterization (e.g.\, force\, velocity\, and amplitude)\, in this talk I will discuss how CSN suppression\, a ubiquitous feature of CSN dynamics across species\, is topographically and temporally organised in motor cortex and how bidirectional CSN output contributes to the execution of task-appropriate actions. \n  \n  \n  \n  \n  \n  \n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/mini-symposium-brain-states-sensory-processing-and-transformation-into-action-in-neurotypical-and-autistic-conditions/
CATEGORIES:For scientists,home-event,Symposium
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241213T140000
DTEND;TZID=Europe/Paris:20241213T140000
DTSTAMP:20260422T094516
CREATED:20241125T133438Z
LAST-MODIFIED:20241125T161334Z
UID:178003-1734098400-1734098400@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Théo Gauvrit
DESCRIPTION:Venue: l’ENSTBB (grosse boule bleu à l’entrée du parking étudiant)\, \nDefense in english \n\nThéo Gauvrit\nNeurocentre Magendie \nThesis supervisor: Andreas Frick \nTitle\nComputational approaches for the analysis and modeling of atypical sensory experience in autism \nAbstract\nHow does the brain encode the perception of sensory stimuli in our environment? This question\, still not fully answered\, becomes even more intriguing in the context of autism\, a neurodevelopmental condition characterized by atypical sensory experience as one of its core symptoms. These sensory alterations\, often manifesting as hyper- or hyporeactivity or variability in sensory responses\, are present in the vast majority of autistic individuals\, have a strong impact on their daily lives\, and contribute to other core symptoms of the condition. Strong neurophysiological alterations in the brain are suspected to drive these symptoms\, but limited research leaves the underlying mechanisms and potential therapeutic targets unclear. We adopted a preclinical translational approach to investigate the neurobiological underpinnings of atypical sensory experience in the tactile domain. This involved recording spontaneous and stimulus-evoked neuronal activity at the single-neuron level in the primary somatosensory cortex (S1) of anesthetized mice of the well-established Fmr1-/y mouse model of autism. This was followed by characterization of the S1 population activity with single-cell resolution in behaving animals during a perceptual decision-making task in the same mouse model. \nExamining spontaneous and stimulus-evoked neuronal activity in single neurons within the S1\, we identified significant trial-by-trial variability in the neuronal responses of Fmr1-/y mice\, a hallmark of atypical sensory processing in autistic individuals. We traced the sources of this variability to increased endogenous neuronal noise\, manifesting as random fluctuations in neuronal activity\, and to network instability\, characterized by rapid\, inconsistent\, and contrasting states. This elevated noise and instability impair the integration of sensory information in the cortex and may contribute to the sensory perception variability observed in clinical studies of autism. Furthermore\, the local (within S1) application of a BKCa channel agonist reduced local neuronal hyperexcitability and corrected many synaptic response features and their variance\, but had little effect on the trial-by-trial variability\, suggesting that this variability and hyperexcitability are less closely coupled than previously thought. \nTo evaluate the impact of these neuronal alterations on tactile detection\, we combined a translational decision-making task (back-translated from human studies) with functional imaging in S1. Our results recapitulated the multifaceted tactile alterations seen in autistic individuals\, with tactile hyposensitivity\, interindividual variability\, and unreliable behavioral responses in Fmr1-/y mice. By examining the evoked activity of pyramidal and GABAergic neurons\, we found that this altered tactile perception could be explained by weak stimulus encoding in S1\, rendering stimulus detection more vulnerable to ongoing network states and thus less reliable. By reducing local hyperexcitability in S1 using an agonist of BKCa channels\, we were able to strengthen stimulus encoding and thus improve tactile detection in Fmr1-/y mice. \nOur results emphasize the critical role of neuronal noise and variability in sensory information processing and the role of hyperexcitability and network states in shaping sensory perception. This translational approach offers mechanistic insight into the neural foundations of atypical tactile perception in autism and underscores the therapeutic potential of targeting these neural mechanisms to enhance sensory sensitivity and reliability in autistic individuals. \nKeywords: Autism\, Perception\, Tactile\, Neuronal Noise\, Cortex \nPublications\nEndogenous noise of neocortical neurons correlates with atypical sensory response variability in the Fmr1−/y mouse model of autism.\nArjun A. Bhaskaran\, Théo Gauvrit\, Yukti Vyas\, Guillaume Bonny\, Melanie Ginger\, Andreas Frick\nNature Communnications 14\, 7905 (2023). https://doi.org/10.1038/s41467-023-43777-z \nStimulus encoding shapes tactile perception and underlies alterations in autism\nbioRxiv 2024.08.08.607129; doi: https://doi.org/10.1101/2024.08.08.607129\nOurania Semelidou\, Théo Gauvrit\, Célien Vandromme\, Alexandre Cornier\, Anna Saint-Jean\, Yves Le Feuvre\, Melanie Ginger\, Andreas Frick \nJury\nRapporteur; M. Brice BATHELLIER; Directeur de Recherche; Université Paris-Cité – INSERM\nRapporteur; Mme. Elizabeth MILNE; Professeure;  University of Sheffield\nExaminateur; M. Ian DUGUID; Professeur; University of Edinburgh;\nExaminateur; Mme. Susanna PIETROPAOLO; Chargée de Recherche; Université de Bordeaux – CNRS \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-theo-gauvrit/
CATEGORIES:Thesis
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DTSTART;TZID=Europe/Paris:20241213T143000
DTEND;TZID=Europe/Paris:20241213T143000
DTSTAMP:20260422T094516
CREATED:20241122T154133Z
LAST-MODIFIED:20241202T155144Z
UID:177932-1734100200-1734100200@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Pierre Mortessagne
DESCRIPTION:Venue: Centre Broca \nDefense in english \n\nPierre Mortessagne\nAbrous’ team\nNeurocentre Magendie \nThesis supervisor: Emilie Pacary \nTitle\nCharacterization of the different populations of granular neurons in the dentate gyrus of the hippocampus: from morphology to function \nAbstract\n\nIn the dentate gyrus (DG) of the hippocampus\, the generation of dentate granule neurons (DGNs) starts during late embryogenesis\, peaks around birth and continues at low levels during adulthood. This continuous neurogenesis makes the DG a unique structure\, composed of DGNs from distinct temporal origins\, which form subpopulations potentially bearing unique anatomical characteristics and functional roles in hippocampal physiology. Surprisingly\, this hypothesis has received limited attention. In this context\, our research aimed to elucidate the morphological\, electrophysiological\, and behavioral characteristics of DGNs subpopulations based on their temporal origin. Building on prior findings from our team that highlighted dendritic differences between these populations\, we focused on examining the features of their axons\, called mossy fibers (MFs). Using sparse labeling strategies — electroporation to target embryonically-born (E14.5) and neonatally-born (P0) DGNs\, and retroviral injections for adolescent-born (P21) and adult-born (P84) DGNs — we uncovered that DGNs generated later in life develop larger MF boutons with more filopodia\, and exhibit a shorter axon initial segment. Additionally\, using the Osteocalcin-Cre and Ascl1CreERT2 mouse lines to selectively label large cohorts of embryonically-born and adult-born DGNs\, respectively\, we found that earlier-born neurons project further onto the CA2 compared to later-born neurons. Following these morphological findings\, we further investigated the functional characteristics of temporally distinct DGNs at both the electrophysiological and behavioral levels. The electrophysiological studies revealed similar intrinsic properties between neonatally- and adult-born DGNs\, and higher basal transmission in neonatally-born DGNs\, potentially reflecting a larger number of active sites. Finally\, we examined the role of embryonic-born DGNs in social behavior\, and showed that acute inhibition of these neurons delayed the expression of social preference. However\, these functional data remain preliminary and need further investigation. Altogether\, this PhD work highlights the significant impact of the birthdate of DGNs on their anatomical and potentially functional characteristics\, and emphasizes the importance of considering their precise temporal origin in any structural or functional analysis of the DG. \nKeywords: Neurogenesis\, Dentate Gyrus\, Dentate Granule Neurons\, Temporal Origin\, Axon \nSélection de publications\nMortessagne P\, Cartier E\, Balia M\, Fèvre M\, Corailler F\, Herry C\, Abrous DN\, Battefeld A\, Pacary E. Genetic labeling of embryonically-born dentate granule neurons in young mice using the PenkCre mouse line. Sci Rep. 2024 Feb 29;14(1):5022. doi: 10.1038/s41598-024-55299-9. \nLods M\, Mortessagne P\, Pacary E\, Terral G\, Farrugia F\, Mazier W\, Masachs N\, Charrier V\, Cota D\, Ferreira G\, Abrous DN\, Tronel S. Chemogenetic stimulation of adult neurogenesis\, and not neonatal neurogenesis\, is sufficient to improve long-term memory accuracy. Prog Neurobiol. 2022 Dec;219:102364. doi: 10.1016/j.pneurobio.2022.102364. \nKerloch T\, Farrugia F\, Bouit L\, Maître M\, Terral G\, Koehl M\, Mortessagne P\, Heng JI\, Blanchard M\, Doat H\, Leste-Lasserre T\, Goron A\, Gonzales D\, Perrais D\, Guillemot F\, Abrous DN\, Pacary E. The atypical Rho GTPase Rnd2 is critical for dentate granule neuron development and anxiety-like behavior during adult but not neonatal neurogenesis. Mol Psychiatry. 2021 Dec;26(12):7280-7295. doi: 10.1038/s41380-021-01301-z. \nLods M\, Pacary E\, Mazier W\, Farrugia F\, Mortessagne P\, Masachs N\, Charrier V\, Massa F\, Cota D\, Ferreira G\, Abrous DN\, Tronel S. Adult-born neurons immature during learning are necessary for remote memory reconsolidation in rats. Nat Commun. 2021 Mar 19;12(1):1778. doi: 10.1038/s41467-021-22069-4. \nJury\n\n\nDr. François GEORGES\, DR – Président\nPr. Flavio DONATO\, Asst. Prof – Rapporteur\nDr. Julien COURCHET\, DR – Rapporteur\nDr. Rosa COSSART\, DR – Examinatrice\nDr. Noelia URBAN\, PI – Examinatrice\nDr. Emilie PACARY\, CR – Directrice de thèse\nDr. Nora ABROUS\, DR – Invitée\nDr. Muriel KOEHL\, DR – Invitée\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-pierre-mortessagne/
CATEGORIES:Thesis
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