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:20241128T100000
DTEND;TZID=Europe/Paris:20241128T100000
DTSTAMP:20260422T074249
CREATED:20241016T101730Z
LAST-MODIFIED:20241016T151731Z
UID:176760-1732788000-1732788000@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Rodrigue Ortolé
DESCRIPTION:Venue : Centre Broca Nouvelle-Aquitaine \n \nThesis defended in french \n\nRodrigue Ortolé\nTeam Dopamine and neuronal assemblies (IMN) \nThesis directed by François Georges \nTitle\nAnatomical and Functional Characterization of Neuronal Projections from the Basolateral Amygdala and Auditory Cortex to the tail of the striatum \nAbstract\nTo understand the anatomo-functional organization of the “auditory striatum\,” we investigated its capacity for multimodal integration. Specifically\, we explored how this structure integrates inputs from the auditory cortex and the basolateral amygdala (BLA)\, a key limbic region crucial for encoding information relevant to fear-related behaviors and anxiety states. Given that the BLA-to-striatum (BLA—TS) pathway remains poorly characterized\, our study aimed to elucidate the anatomo-functional organization of these two key pathways\, with a focus on their interaction with the dopaminergic innervation of the TS. \nWe first sought to dissect the projections from the BLA and auditory cortex (AUV) to the TS using retrograde and anterograde tracing techniques. Our findings demonstrate that the TS receives inputs from the amygdala of both hemispheres\, with a predominant contribution from the ipsilateral BLA. For the AUV\, the majority of TS innervation also originates from the ipsilateral side. We further mapped the projection patterns of these pathways\, showing that BLA neurons primarily target the dorsal and ventrolateral regions of the TS\, areas enriched in tyrosine hydroxylase (TH). In contrast\, AUV neurons mainly project to the ventral TS. Additionally\, we observed that the BLA-TS pathway does not innervate PV interneurons\, contrary to the AUV-TS pathway. \nRegarding dopaminergic innervation\, our results reveal multiple sources\, with most inputs arising from the substantia nigra pars compacta (SNc) but also from the substantia nigra pars lateralis (SNL) and ventral tegmental area (VTA) in roughly equal proportions. This finding was confirmed through selective lesioning of dopaminergic neurons. \nFinally\, we assessed the functional connectivity of these pathways using fiber photometry and provided functional evidence of their connectivity through electrical stimulation. Robust responses in the TS were recorded following stimulation of both the BLA and AUV. Additionally\, we compared the evoked responses between the ipsilateral and contralateral BLA inputs\, as well as between the AUV and BLA pathways. \nOverall\, this study offers a detailed anatomical characterization of the AUV and BLA inputs to the TS\, as well as the multiple origins of dopaminergic innervation. Functionally\, it also allowed for a comparison of the glutamatergic inputs to the TS and their distinct roles in modulating striatal activity. \nKey words\n\nTail of the striatum\, amygdala\, auditory cortex\, dopamine\, fiber photometry\, functional connectivity \nPublications\n\nWalle R\, Petitbon A\, Fois GR\, Varin C\, Montalban E\, Hardt L\, Contini A\, Angelo MF\, Potier M\, Ortole R\, Oummadi A\, De Smedt-Peyrusse V\, Adan RA\, Giros B\, Chaouloff F\, Ferreira G\, de Kerchove d’Exaerde A\, Ducrocq F\, Georges F\, Trifilieff P. Nucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure. Nat Commun. 2024 Mar 21;15(1):2543. doi: 10.1038/s41467-024-46874-9. PMID: 38514654; PMCID: PMC10958053\n\nJury\nDr. BELUJON Pauline\, MCU\, INSERM\, Université de Poitier – Rapporteur\nDr. VEINANTE Pierre\, Professeur\, CNRS\, Université de Strasbourg – Rapporteur\nDr. LE MOINE Catherine\, DR\, CNRS\, Université de Bordeaux  – Examinatrice\nDr. VALJENT Emmanuel\, DR\, CNRS\, Université de Montpellier – Examinateur \n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-rodrigue-ortole/
CATEGORIES:IMN,Thesis
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241128T140000
DTEND;TZID=Europe/Paris:20241128T140000
DTSTAMP:20260422T074249
CREATED:20241106T140243Z
LAST-MODIFIED:20241125T145356Z
UID:177271-1732802400-1732802400@www.bordeaux-neurocampus.fr
SUMMARY:Thesis Defense - Xuesi Zhou
DESCRIPTION:Venue: Centre Broca \n\nXuesi Zhou \nTeam Giannone – IINS\nThesis directors: Grégory Giannone (IINS) & Brahim Louinis (LP2N) \nTitle\nDeciphering the mechano-properties of the membrane periodic skeleton in neurons using super-resolution microscopy\n(Déchiffre les propriétés mécaniques du squelette périodique de la membrane dans les neurones à l’aide de la microscopie à super-résolution) \nAbstract\nMechanotransduction is the detection of mechanical forces by cells and their conversion into biochemical signals. Mechanotransduction events is key for regulating neuronal functions during physiological processes\, such as development and synaptic transmission\, and pathophysiological events\, including traumatic brain injury and neurodegeneration\, or during aging. Axons experience forces during limb flexion\, but also during interactions with post-synapses and neuroglia in brain. The membrane periodic actin-spectrin skeleton (MPS) of axons\, revealed by super-resolution with a period of approximately 190 nm\, could play a crucial role in neuron mechanosensing. ab-spectrin tetramers within MPS can theoretically extend under force. The MPS is also composed of adhesion\, actin-binding and signaling proteins (such as Src\, CB1)\, some identified as mechanosensors of non-neuronal cells. \nMy PhD aims to uncover whether the MPS in axons is a mechano-sensitive structure by studying the mechanical response and reorganizations of its components at molecular level. We recently developed the only cell stretching device compatible with super-resolution microscopy\, allowing to capture the acute mechanical response of individual proteins inside mechanosensitive structures. We first adapted the stretching device to neurons to image the MPS by super-resolution and quantified its molecular deformations and reorganizations after stretch. We then applied a 30% stretch to axons at different rates (0.1s\, 1s\, 100s). Fast stretch (0.1s\, 1s) induced increased period of spectrin and MPS irreversible plastic deformation (0.1s) or MPS reversible elastic deformation (1s)\, while slow stretch (100s) did not alter spectrin period. Thus\, the MPS is a resilient mechanosensitive structure\, but extreme fast deformations disrupt its molecular organization. We also revealed the mechano-dependent dissociation of adducin (actin capping protein)\, demonstrating an active molecular reorganization of the MPS. We are confident that\, we will be able to obtain all the results to demonstrate for the first time that the MPS is a mechanosensitive structure responding to force through reorganization of spectrin and actin-binding proteins. \nIn collaboration with the group of Christophe Lamaze at Institut Curie (Paris\, France)\, we adapted our strategy to assessed the impact of mechanical stretching in caveolin nanoscale reorganization in endothelial cells\, using super-resolution. \n  \nKeywords: mechanosensing\, axon\, membrane periodic skeleton\, spectrin\, cell stretching\, super resolution microscopy \nJury\n\nChristophe Leterrier\, INP (Rapporteur)\nMarina Mikhaylova\, HU Berlin (Rapporteur)\nPierre Nassoy\, LP2N (Examiner)\nNils Gauthier\, IFOM (Examiner)\nFrancesca Pennacchietti\, KTH (Examiner)\nBrahim Louis\, Université de Bordeaux (Director)\nGrégory Giannone\, IINS (Co-director)\nAnna Brachet\, IINS (Guest)\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-xuesi-zhou/
CATEGORIES:Thesis
END:VEVENT
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241128T140000
DTEND;TZID=Europe/Paris:20241128T140000
DTSTAMP:20260422T074250
CREATED:20241115T115750Z
LAST-MODIFIED:20241125T145338Z
UID:177673-1732802400-1732802400@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Jeflie Tournezy
DESCRIPTION:Venue: Salle de conférence Neurocentre Magendie \n\nDefense in french \nJeflie Tournezy\nTeam: Oliet\, Neurocentre Magendie \nThesis supervisor: Stéphane Chevallier \nTitle\nTherapeutic effects of the Borna virus X protein in SOD1G93A mice \nAbstrac\nToday\, Amyotrophic Lateral Sclerosis (ALS) remains an incurable disease for which therapeutic trials have been unsuccessful. It is therefore essential to propose new therapeutic approaches that would slow the progression of the disease and prolong patient survival. \nAmong the pathophysiological characteristics described\, mitochondrial dysfunctions are one of the earliest events and could be the origin of the progressive loss of motor neurons. Restoring mitochondrial functions could therefore constitute a therapeutic area of interest to develop new therapies against this disease. \nWith this in mind\, we were interested in the X protein of the Bornavirus (BDV for Borna Disease Virus). When it targets mitochondria\, the X protein inhibits the apoptosis of neurons and protects them from degeneration in an animal model of Parkinson’s disease (Szelechowski et al.\, 2014). This neuroprotective action of the X protein resides in its last 29 carboxy-terminal amino acids which constitute the PX3 peptide. In addition\, a modification to increase the mitochondrial localization of the protein X (XA4 protein) has shown improved neuroprotective effects in vitro. \nThis thesis aimed to propose a new preclinical therapeutic approach\, consisting in protecting motor neurons by using the neuroprotective properties of the Bornavirus X protein. \nFirst\, we tested the neuroprotective effects of the X protein and its derived peptide PX3 in a well-characterized model of ALS\, the SOD1G93A mice. Administration of the PX3 intranasally and the X intramuscularly via a viral vector (CAV2-X) slowed the progression of the disease and increased the survival of lumbar motor neurons. However\, this treatment did not increase the life expectancy of the mice. \nThen\, we used adeno-associated viruses (AAV) as gene transfer tools. More specifically\, we used AAV serotype 10 (AAV10) to administer the gene encoding the X protein (AAV10-X) or its modified form\, the XA4 protein (AAV10-XA4) to SOD1G93A mice. We evaluated the effects of these treatments on motor performances\, life span\, denervation of the neuromuscular junction\, and preservation of lumbar and phrenic motor neurons (motor neurons innervating the diaphragm). \nOur results show that the X and XA4 proteins slowed the degeneration of lumbar motor neurons. Furthermore\, while the X protein delayed the onset of motor deficits\, the XA4 protein extended the life expectancy of the animals. The maintenance of motor performances in mice treated with X protein was associated with better preservation of the neuromuscular junction compared to untreated SOD1G93A mice. \nIn addition\, the administration of X or XA4 proteins to SOD1G93A mice blocks the degeneration of phrenic motor neurons\, allowing them to return to values like the wild-type group. \nAlthough further investigations are needed to better understand the mechanisms involved in the effects of these proteins\, our work demonstrates their certain therapeutic effects\, on the extension of the life span\, on the preservation of the neuromuscular junction\, and the limitation of the degeneration of the spinal motor neurons. These studies open a new therapeutic avenue against ALS. \nKey words: amyotrophic lateral sclerosis; SOD1G93A mice; motor neuron degeneration; motor tests; life span \nJury\nM. RAOUL\, Cédric – Directeur de recherche-Université de Montpellier – INSERM U1051 – rapporteur \nMme BERTRAND\, Sandrine – Directrice de recherche-Université de BORDEAUX – examinatrice \nM. GOIZET\, Cyril – Praticien hospitalier – Bordeaux- examinateur \nMme CHEVALLIER\, Stéphanie – Maitre de conférences – Université Bordeaux – directrice de thèse \nM. LE MASSON Gwendal Professeur-Praticien hospitalier-Bordeaux-membre invité \nMembres invités :\n \nMme DA CRUZ\, Sandrine-Directrice de recherche- Leuven Brain Institute Belgique-examinatrice \nM. ROBITAILLE\, Richard-Directeur de recherche-Université de Montréal- rapporteur \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-jeflie-tournezy/
CATEGORIES:Thesis
END:VEVENT
END:VCALENDAR