BEGIN:VCALENDAR
VERSION:2.0
PRODID:-//Bordeaux Neurocampus - ECPv4.9.10//NONSGML v1.0//EN
CALSCALE:GREGORIAN
METHOD:PUBLISH
X-WR-CALNAME:Bordeaux Neurocampus
X-ORIGINAL-URL:https://www.bordeaux-neurocampus.fr/en/
X-WR-CALDESC:Events for Bordeaux Neurocampus
BEGIN:VTIMEZONE
TZID:Europe/Paris
BEGIN:DAYLIGHT
TZOFFSETFROM:+0100
TZOFFSETTO:+0200
TZNAME:CEST
DTSTART:20240331T010000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20241027T010000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241206T090000
DTEND;TZID=Europe/Paris:20241206T090000
DTSTAMP:20260422T094411
CREATED:20241129T144101Z
LAST-MODIFIED:20241129T144617Z
UID:178183-1733475600-1733475600@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Axel Palaude
DESCRIPTION:Venue : Centre Broca Nouvelle-Aquitaine\, salle de réunion Pyramide\, IINS\nZoom : https://u-bordeaux-fr.zoom.us/j/7761081719?omn=84507465728 \nThesis defended in french \n\nAxel Palaude\nIMN\nThesis directed by Thierry Vieville \nTitle\nStrategies for problem-solving : a model to classify problem-solving behaviours \nAbstract\nLearning regulation is the set of skills that facilitate learning. This includes motivational and emotional skills\, as well as meta-cognition skills\, such as monitoring goals and strategies. Learning situations are present in every-day life\, and mostly take the form of open problems\, problems for which there is an unknown solution or method to achieve them. Open problem solving requires learning unknown elements\, which requires regulation skills. Understanding the strategies used by learners to solve open-ended problems allows us to better understand the regulation processes and therefore the learning process. Regulatory processes can be influenced and trained\, and this understanding of the processes could lead\, to better-suited teaching methods. This thesis presents a model representing the learning process of a learner confronted with an open problem\, as well as a method allowing\, based on external observations of actions carried out by learners\, to group problem-solving sequences depending on the strategies used. The analysis methods use clustering algorithms\, which using dynamic time warping as a measure of similarity between problem-solving sequences. This dynamic time warping measure is applied to symbolic data\, which can be compared through the use of proper metrics. In the context of small datasets\, a metaclustering method is presented for robustness purposes. Two case studies use the method defined here to show the potential uses of such a method but also to discuss its limitations. The first\, CreaCube\, is the study of a creative problem-solving task\, in which we try to understand the processes of creativity. Second\, Outer Wilds tries to extend the analysis to long problems. \nKey words\nCreative problem solving\, Strategies\, Regulation\, Dynamic Time Warping \nJury\nMme Sophie MORLAIX (rapportrice)\nMme Iza MARFISI (rapportrice)\nM. Gayo DIALLO (président du jury)\nMme Morgane CHEVALIER (examinatrice)\nM. Yann SECQ (examinateur) \n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-axel-palaude/
CATEGORIES:IMN,Thesis
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241206T093000
DTEND;TZID=Europe/Paris:20241206T093000
DTSTAMP:20260422T094411
CREATED:20241007T075145Z
LAST-MODIFIED:20241025T152827Z
UID:176264-1733477400-1733477400@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Paul Lapios
DESCRIPTION:Venue: CARF \n\nPaul Lapios\nPerrais’ team  (IINS)\nThesis supervisor: David Perrais \nTitle\nUltrastructural and molecular analysis of cortico-striatal dopamine hub synapses \nAbstract\nDopamine is a neurotransmitter that modulates neuronal activity and governs essential functions such as reward prediction\, motivation\, and motor control. In the striatum\, dopamine typically acts over a large volume through slow-acting metabotropic receptors. However\, recent studies have demonstrated that dopamine can also operate in localized hotspots measuring a few cubic micrometers. Additionally\, dopamine may trigger excitatory synapse potentiation when released in synchrony with glutamate. Despite these advances\, molecular and ultrastructural studies have been limited by technical challenges. \nDuring my doctoral training\, I developed cutting-edge techniques to explore the molecular and ultrastructural features of dopaminergic terminals and their relationship to synapses in the mouse striatum. \nIn a first piece of work\, we aimed at analyzing the composition of dopaminergic (DA) terminals. To that end\, we labeled dopaminergic neurons with a green fluorescent reporter under the control of the Dopamine Transporter promoter (DAT-cre line). Following subcellular fractionation of the striatum\, we isolated green fluorescent synaptosomes (resealed terminals bound to synaptic partners) with fluorescence-activated synaptosome sorting (FASS). Immunolabeling of these isolated DA synaptosomes confirmed the presence of genuine dopaminergic markers apposed to dopamine receptors. Surprisingly\, 30% of dopamine synaptosomes were bound to cortico-striatal excitatory synapses expressing the type 1 vesicular glutamate transporter (GLU). We termed these connections cortico-striatal dopamine hub synapses (DHS). On these samples\, I used 6 markers of the GLU pre- and post-synapse to scrutinize the effect of the association in DHS. I could identify that the association in DHS corelates with a molecular remodeling of the cortico-striatal synapses (1). Dopamine hub synapses may thus serve as a structural substrate for localized dopamine activity in the striatum and could further potentiate glutamatergic signaling. \nNext\, I established a cryo-correlative light and electron microscopy (cryo-CLEM) protocol on labeled synaptosomes to determine the ultrastructure of dopamine terminals and DHS in three dimensions. Compared to cortico-striatal pre-synapses\, DA synaptosomes were three times smaller and contained ten times fewer synaptic vesicles (SVs). The size and shape of SVs in DA terminals were more heterogeneous; they were generally larger and sometimes elongated. While GLU synapses exhibited active zones (AZ) and postsynaptic densities\, DA terminals lacked distinct vesicle clusters or clear synaptic organization. Only 35% of dopamine terminals contained at least one tethered SV required for exocytosis. In these terminals\, SVs were more abundant and closer to the plasma membrane\, suggestive of a higher release activity. However\, primed SVs (tethered within 5 nm of the plasma membrane) were absent. Interestingly\, GLU terminals in DHS had more primed SVs compared to regular GLU synapses\, implying that the presence of DA terminals reorganizes SVs in glutamatergic terminals. These results suggest that the interaction of DA terminals with synapses modifies the release properties of GLU pre-synapses by a local dopamine-dependent plasticity (2). \nGiven that dopamine dysregulation is implicated in addiction and Parkinson’s disease (for which effective treatments are limited)\, the discovery of this multipartite structure responsible for specific dopamine activity on glutamatergic inputs represent a new conceptual framework for future studies in the field. Modulating the physical interaction between DA and GLU synapses in vivo could provide a new method to influence dopamine signaling in the striatum. \nKeywords: Synapse\, Dopamine\, Synaptic plasticity\, Striatum\, Cryo-CLEM \nPublications\n(1)   Paget-Blanc V et al.\, (2022) A synaptomic analysis reveals dopamine hub synapses in the mouse striatum. Nat Commun 13:3102 \n(2)   Paul Lapios\, Robin Anger\, Vincent Paget-Blanc\, Vladan Lučić\, Rémi Fronzes\, Etienne Herzog#\, and David Perrais# (2024) In preparation \nJury\n\nAude Panatier (University of Bordeaux)\nIra Milosevic (University of Oxford)\nBenoit Zuber (University of Bern)\nJean-Antoine Girault (Sorbonne University)\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-paul-lapios/
CATEGORIES:Thesis
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241206T113000
DTEND;TZID=Europe/Paris:20241206T113000
DTSTAMP:20260422T094411
CREATED:20240710T165938Z
LAST-MODIFIED:20250623T161331Z
UID:173127-1733484600-1733484600@www.bordeaux-neurocampus.fr
SUMMARY:PhD seminar - Mathieu Bourdenx
DESCRIPTION:Venue: Centre Broca \nOpen to everyone! \n\nMathieu Bourdenx\, PhD\nSenior Research Fellow\nUCL\, London\, UK \nMathieu Bourdenx was a PhD student in Erwan Bezard’s team in 2012-2016.  \nTitle\nFrom organelles to cell-types: understanding proteostasis dysfunction in ageing and neurodegeneration \nAbstract\nAll cells count on surveillance systems that assure the maintenance of their proteome. Protein quality control decreases with age contributing to the vulnerability of specific cell populations to pathogenic proteins\, such as tau. In this talk\, I will discuss two complementary projects. First\, I will focus on subcellular proteomic analyses of samples from Alzheimer’s disease patients. This unique dataset demonstrates that protein localization dominates over changes in abundance\, an aspect that has been vastly overlooked. We have identified\, organelle-specific\, molecular signatures correlating with tau pathogenic activity\, providing new avenues for biomarker development. In the second part of my talk\, I will change scale and focus on how brain cell-types are affected by the process of ageing. Combining spatial transcriptomics and single-cell genomics\, we have identified neuronal populations uniquely vulnerable to ageing-related proteostasis blockage. Comparing these vulnerable populations to their closest-related resilient cousins allowed to identify novel mechanisms of vulnerability\, which are now investigated for modulation. \nKey publications\n\nWatamura N\, Foiani M\, Bez S\, Bourdenx M\, et al. In vivo hyperphosphorylation of tau is associated with synaptic loss and behavioral abnormalities in the absence of tau seeds. Nature Neuroscience (in press)\nBourdenx M\, et al. Chaperone-mediated autophagy prevents collapse of the neuronal metastable proteome. Cell. 2021 May 13;184(10):2696-2714.e25. doi: 10.1016/j.cell.2021.03.048.\nCaballero B*\, Bourdenx M*\, et al. Acetylated tau inhibits chaperone-mediated autophagy and promotes tau pathology propagation in mice. Nat Commun. 2021 Apr 14;12(1):2238. doi:10.1038/s41467-021-22501-9.\nKirchner P\, Bourdenx M\, Madrigal-Matute J\, Tiano S\, Diaz A\, Bartholdy BA\, Will B\, Cuervo AM. Proteome-wide analysis of chaperone-mediated autophagy targeting motifs. PLoS Biol. 2019 May 31;17(5):e3000301. doi: 10.1371/journal.pbio.3000301.\nBourdenx M\, et al. Identification of distinct pathological signatures induced by patient-derived α-synuclein structures in nonhuman primates. Sci Adv. 2020 May 13;6(20):eaaz9165. doi:10.1126/sciadv.aaz9165.\n\nMeet the speaker!\nYou are a research staff ? Write to Julia Goncalves who will organize the schedule. \nYou are a PhD student? You can register to share some pizza after the talk. Registration opens 3 weeks before. \n\nPhD seminars are organized by the NBA\, Bordeaux Neurocampus\, and the Bordeaux Neurocampus Graduate Program.  \n \n
URL:https://www.bordeaux-neurocampus.fr/en/event/phd-seminar-mathieu-bourdenx/
CATEGORIES:For scientists,home-event,Monthly conferences
END:VEVENT
END:VCALENDAR