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X-WR-CALDESC:Events for Bordeaux Neurocampus
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DTSTART;TZID=Europe/Paris:20241218T090000
DTEND;TZID=Europe/Paris:20241218T090000
DTSTAMP:20260422T095438
CREATED:20241205T104644Z
LAST-MODIFIED:20241205T110633Z
UID:178408-1734512400-1734512400@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Ifrah Omar Ibrahim
DESCRIPTION:Venue: BBS \n\nIfrah Omar Ibrahim\nRMSB – Team Metapat\nhttps://www.rmsb.u-bordeaux.fr/fr/la-recherche/equipe-metapat/ \nSupervisor: Anne-Karine Bouzier-Sore \nTitle\nLactate and Hypothermia: A Dual Approach for Neuroprotectionin Neonatal Hypoxia-Ischemia \nAbstract\nSince the introduction of the astrocyte-neuron lactate shuttle (ANLS) concept by Pellerin and Magistretti in 1994\, it has been proposed that lactate produced by astrocytes via glycolysis is transferred to neurons as a preferred energy substrate. More recently\, the critical role of ANLS in brain activation and its associated functions has been demonstrated in vivo. Given that lactate is essential for neuronal activity\, the question arises: could it also be neuroprotective in conditions characterized by cerebral energy deficits? To address this question\, we used a neonatal hypoxia-ischemia (NHI) model\, a leading cause of mortality and subsequent disabilities in infants. NHI results in brain lesions due to a significant reduction in oxygen (O2) and glucose supply. Currently\, the only clinical treatment is moderate therapeutic hypothermia (TH)\, which helps limit the neurological damage caused by NHI. However\, nearly half of the affected newborns do not respond favorably to this treatment. \nResearch conducted by our team using an NHI rat model demonstrated that lactate administration has neuroprotective effects. The aim of my thesis was to determine whether lactate administration is compatible with HT following an NHI event and to compare the effects of combining these two therapies with HT alone. To achieve this goal\, my thesis was structured around three main objectives: \n\nDevelopment of a hypothermia protocol in an NHI rat model: This was done to identify optimal treatment conditions. Three hypothermia durations (2 h\, 3 h\, and 5 h) post-NHI were compared through longitudinal monitoring of brain damage using MRI (Bruker 4.7T) and various behavioral tests. Histological and immunohistochemical analysis were also conducted to provide complementary insights.\nEvaluation of the therapeutic potential of lactate combined with hypothermia: The neuroprotective effects of this combination were compared to TH alone. The optimal window for lactate administration was also established. The molecular mechanisms underlying these neuroprotective effects were investigated using Western blot analysis. Additionally\, the impact of lactate on neuroinflammation was examined by evaluating its role in modulating microglial phenotypes.\nAssessment of the safety of lactate administration on neonatal blood parameters: This was conducted through a retrospective study of preterm infants who received sodium L-lactate infusions.\n\nOur findings clearly indicated that 2 hours of TH were sufficient to reduce brain lesion volumes and achieve optimal performance in behavioral tests. Moreover\, lactate administration combined with TH proved to be more neuroprotective than TH alone. Finally\, in the retrospective study\, sodium L-lactate infusion in preterm infants did not increase lactatemia or disturb other blood parameters. \nIn conclusion\, lactate administration is neuroprotective in the context of NHI\, even when combined with TH\, and is safe for preterm infants\, even when lactatemia is already elevated. These results suggest promising potential for clinical pediatric applications. \nKey words : Brain metabolism\, lactate\, neonatal hypoxia-ischemia\, MRI\, behavior\, hypothermia. \nJury\n\nMme. Anne-Karine BOUZIER-SORE\, Directrice de Recherche CNRS / Université de Bordeaux  – Directrice de thèse\nMme. Rosa Chiara PAOLICELLI\, Professeure associée / Université de Lausanne – Rapporteure\nLaurent SUISSA\, Professeur des Universités – Praticien Hospitalier / Université d’Aix-Marseille – Rapporteur\nRémy GUILLEVIN\, Professeur des Universités – Praticien Hospitalier / Université de Poitiers – Examinateur\nMme. Émilie PACARY\, Chargée de Recherche Inserm / Université de Bordeaux – Examinatrice\nSylvain MIRAUX\, Directeur de Recherche CNRS / Univeristé de Bordeaux – Invité\nLuc PELLERIN\, Professeur des Universités – Praticien Hospitalier / Université de Poitiers – Invité\nMme. Hélène ROUMES\, Chargée de Recherche CNRS / Université de Bordeaux – Invitée\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-ifrah-omar-ibrahim/
CATEGORIES:Thesis
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DTSTART;TZID=Europe/Paris:20241218T120000
DTEND;TZID=Europe/Paris:20241218T120000
DTSTAMP:20260422T095438
CREATED:20241205T172358Z
LAST-MODIFIED:20241209T174407Z
UID:178643-1734523200-1734523200@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Sandra Beriain
DESCRIPTION:The defense is taking place in Bilbao \n\nSupervisors: Giovanni Marsicano (Magendie) and Elena Vecino (Universidad del Pais Vasco) \nTitle\nRoles of the CB1 receptor and the endocannabinoid system in the retina \nAbstract\nThe retina\, a sensory extension of the central nervous system\, transforms light into electrical signals for visual processing\, involving intricate neuronal and glial interactions. Key retinal neurons such as photoreceptors\, bipolar\, horizontal\, amacrine\, and ganglion cells\, coordinate visual signal transmission\, supported by Müller glia\, which provide structural and metabolic aid. Retinal disorders\, including glaucoma and diabetic retinopathy\, cause irreversible blindness through neuronal degeneration. \nThe endocannabinoid system (ECS)\, a neuromodulatory network comprising cannabinoid receptors (CB1 and CB2)\, endocannabinoids\, and enzymes for their synthesis and degradation\, plays a pivotal role in modulating brain and body functions. In particular\, the ECS is involved in retinal function and health\, influencing neurotransmission\, visual processing\, and cellular communication. Its role in both normal physiology and pathological conditions highlights the therapeutic potential of cannabinoids in treating retinal disorders. However\, the involvement of the endocannabinoid system in Müller glia\, as well as the different roles of the CB1 receptor\, particularly in retinal metabolism\, vision dependent behaviours\, and response to pathological insults\, remains largely unexplored. This study investigated ECS roles in retinal function and pathology. CB1 receptors were localized predominantly in the inner and outer plexiform layers\, overlapping with markers for photoreceptors\, bipolar\, horizontal\, amacrine\, and ganglion cells. Müller glia were confirmed to express all ECS components and synthesize endocannabinoids\, primarily 2-arachidonoylglycerol\, highlighting their role in neuron-glia communication mediated by cannabinoid signaling. Functionally\, CB1 receptor activation reduced mitochondrial oxygen consumption in retinal homogenates\, suggesting a regulatory role in retinal energy metabolism. In addition\, behavioral tests revealed that CB1 receptors are critical for processing visual stimuli related to defensive behaviors\, such as detecting looming threats\, but are not required for spatial navigation or auditory-cue-driven fear responses. Finally\, in pathological contexts\, CB1 constitutive deletion showed no direct impact on retinal ganglion cell survival after ischemia/reperfusion injuries. \nOverall\, the findings underscore the ECS as integral to retinal health\, with roles in synaptic modulation\, metabolism\, and visually evoked behaviors. The identification of Müller glia as active participants in ECS signaling broadens understanding of neuron-glia interactions. These insights open avenues for therapeutic exploration of cannabinoids in retinal diseases. \nJury\n\nPedro de la Villa (University of Alcalá)\nNagore Puente (University of the Basque Country)\nGuillaume Ferreira (University of Bordeaux)\nFrank Kirchhoff (Saaland University)\nand Stefanie Hauck (Helmholtz Zentrum München).\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-sandra-beriain/
CATEGORIES:Thesis
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241218T140000
DTEND;TZID=Europe/Paris:20241218T140000
DTSTAMP:20260422T095438
CREATED:20241008T132302Z
LAST-MODIFIED:20241008T133007Z
UID:176508-1734530400-1734530400@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Sarah Bou Sader Nehme
DESCRIPTION:Venue : Centre Broca Nouvelle-Aquitaine \n \nThesis defended in English \n\nSarah Bou Sader Nehme\nIMN\nThesis directed by Marc Landry and Walid Hleihel \nTitle\nCortical mechanisms of comorbidity between pain sensitization and attention-deficit/hyperactivity disorder (ADHD) in a mouse model \nAbstract\nAttention deficit/hyperactivity disorder (ADHD) and chronic pain are two complex conditions of multifactorial origins. Clinical and preclinical studies support an association between these two syndromes. However\, the mechanisms underlying their comorbidity are not well understood. Previous findings from our team demonstrated a hyperactivity of the neurons of the anterior cingulate cortex (ACC) and a deregulation of the ACC-posterior insula (PI) pathway in ADHD-like conditions. Growing evidence also suggests a role for neuroinflammation in this concomitance. Our hypothesis thus suggests that neuroinflammation triggers an enhanced neuronal activity in the ACC that sensitizes pathways involved in ADHD symptoms and pain perception. Therefore\, this Ph.D. work aims to elucidate the inflammatory mechanisms that may underlie ADHD and its associated pain sensitization\, with an interest in the role of the purinergic P2X4 receptor. \nTo address this question\, we generated an ADHD-like mouse model through the unilateral intracerebroventricular injection of 6-hydroxydopamine (6-OHDA) at P5. Two-month-old wild-type male and female mice were sacrificed\, their brains were extracted\, and their ACC and PI were dissected. Fixed tissues were used to study microglial and astrocytic morphology while fresh tissues were utilized for transcriptomic\, proteomic\, and phosphoproteomic investigations. Moreover\, mice with a total knock-out of the P2X4 receptor were tested for thermal and mechanical pain sensitization\, in addition to hyperactivity. Fixed tissues of the ACC were used to study changes in microglial morphology while fresh tissues of the ACC and PI were utilized for transcriptomic analyses. \nRegarding the identification of inflammatory mechanisms in our ADHD-like mouse model\, our results report (i) changes in microglial and astrocytic morphology\, associated with cellular reactivity\, in the ACC of 6-OHDA mice\, (ii) the presence of a pro-inflammatory environment in the ACC and PI of 6-OHDA mice\, (iii) modifications in protein expression and kinase (serine-threonine and tyrosine) activity in the ACC and PI of 6-OHDA mice\, and correlated with impairments in axon guidance\, apoptosis\, cytoskeleton dynamics\, signaling cascades\, neurotrophins\, and neurotransmitter systems\, and (iv) alterations in protein interactions and\, therefore\, neuronal-astrocytic communication in the ACC of 6-OHDA mice. Finally\, data integration identified four processes impaired in the ACC and PI of 6-OHDA males and females: apoptosis\, axon guidance\, synaptic plasticity (long-term potentiation)\, and growth of neuronal components. Interestingly\, alterations in these processes were not only linked to ADHD and chronic pain conditions but also associated with Eph/ephrin bidirectional signaling cascades. Our findings also indicate a role for the P2X4 receptor in the worsening of ADHD hyperactivity symptom and the induction of morphological changes in microglial cells that correlate with cellular reactivity. However\, it exerts a protective effect by limiting the expression of pro-inflammatory molecules\, possibly from non-microglial cells. \nIn conclusion\, our work provides interesting insights into the inflammatory mechanisms that may underpin the comorbidity between ADHD and pain sensitization. A mild and sustained pro-inflammatory environment in the ACC and PI drives changes in synaptic-related (long-term potentiation\, axon guidance\, outgrowth of neuronal components) and apoptotic processes. These impairments alter cell-cell connectivity and neuronal activity\, thus participating in ADHD and chronic pain pathogenesis. \n  \nKey words\nCortical mechanisms\, ADHD\, pain sensitization\, neuroinflammation\, anterior cingulate cortex\, insular cortex \nJury\nMme NADJAR Agnès\, Professeure\, Université de Bordeaux\, Présidente du jury\nM. GLENNON Jeffrey\, Docteur\, University College Dublin\, Rapporteur\nMme SÁNCHEZ-PÉREZ Ana-María\, Professeure\, University Jaume I\, Rapportrice\nMme BITAR Tania\, Docteure\, Université Saint-Esprit Kaslik\, Examinatrice\nM. GALINEAU Laurent\, Docteur\, Université de Tours\, Examinateur\nMme RÉAUX-LE-GOAZIGO Annabelle\, Directrice de recherche INSERM\, Examinatrice\nM. LANDRY Marc\, Professeur\, Université de Bordeaux\, Directeur de thèse\nM. HLEIHEL Walid\, Professeur\, Université Saint-Esprit Kaslik\, Directeur de thèse \nPublications\n\nBou Sader Nehme\, S.\, Sanchez-Sarasua\, S.\, Adel\, R.\, Tuifua\, M.\, Ali\, A.\, Essawy\, A. E.\, Abdel Salam\, S.\, Hleihel\, W.\, Boué-Grabot\, E.\, & Landry\, M. (2024). P2X4 signalling contributes to hyperactivity but not pain sensitization comorbidity in a mouse model of attention deficit/hyperactivity disorder. Frontiers in pharmacology\, 14\, 1288994. https://doi.org/10.3389/fphar.2023.1288994\nAssaf\, M.\, Rouphael\, M.\, Bou Sader Nehme\, S.\, Soufia\, M.\, Alameddine\, A.\, Hallit\, S.\, Landry\, M.\, Bitar\, T.\, & Hleihel\, W. (2024). Correlational Insights into Attention-Deficit/Hyperactivity Disorder in Lebanon. Int. J. Environ. Res. Public Health\, 21\, 1027. https://doi.org/10.3390/ijerph21081027\nBou Sader Nehme\, S.\, Sanchez-Sarasua\, S.\, Dhellemmes\, T.\, Tuifua\, M.\, Hleihel\, W.\, Landry\, M. (2024). Neuroinflammation et mécanismes spinaux de la douleur (under review)\n\n  \n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-sarah-bou-sader-nehme/
CATEGORIES:IMN,Thesis
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20241218T140000
DTEND;TZID=Europe/Paris:20241218T140000
DTSTAMP:20260422T095438
CREATED:20241122T154256Z
LAST-MODIFIED:20241202T153100Z
UID:177951-1734530400-1734530400@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Simon Boylan
DESCRIPTION:Venue: BBS\nLien zoom : https://u-bordeaux-fr.zoom.us/j/8733956580\n \n\nSimon Boylan\nINCIA \nThesis supervisor: Alexandre Zénon \nTitle\nCognitive effort\, efficient coding and non-invasive fMRI measurement of their relation in sensorimotor responses \nAbstract\nCognitive effort is a ubiquitous subjective feeling of exertion that pushes people to avoid demanding tasks. From a biological and evolutionary point of view\, mental effort is thought to be a mechanism intended to preserve cognitive resources. However\, so far\, no consensus on the nature of these resources has been established. Since the brain functions as an information-processing organ\, efficient coding theory suggests that cognitive resources — whatever their nature — are optimized and should depend on information gain.\nThis hypothesis assumes certain principles about neural coding and information processing. Firstly\, we frame our work in the premise that the brain is a Bayesian information-processing machine\, that updates internal models through inferences between inputs and previous beliefs. If stimuli are familiar and naturalistic\, efficient neural coding can take place to optimize information coding and processing. If these conditions are met\, then we can estimate the quantity of information computed by the brain as the relative entropy between prior and posterior beliefs\, or information gain; moreover the quantity of energy needed to compute information being optimized\, energy spent on a task should be proportional to this same quantity.\nIndirect measures of this relationship have been validated through pupillometry\, as pupil size correlates with information rate during cognitive tasks. In this thesis\, we designed experiments to further validate this information-theoretic framework\, using complementary behavioral and neuroimaging measures. To assess this hypothesis\, we conducted three key experiments : two joystick visuo-motor and oculo- motor tracking tasks with pupillometry\, and a response-to-stimulus (Hick-Hyman) task in fMRI. \nThe first study investigates the relation between cognitive effort\, pupil-size and continuous visual-motor prediction under this information framework. By controlling information components of the target\, such as predictability\,  lag\, speed and acceleration\, we can validate the information origin of cognitive effort (NASA-TLX) and its correlation with pupil-size. \nThe second experiment was developed to test the overnight memorization and implicitness of eye and hand continuous tracking. Using the same design as in the first experiment\, we ran four experimental sessions\, divided in joystick and eye tracking\, on two consecutive days. We showed that participants implicitly learned to better predict repeating parts of the trajectory\, which resulted in better performance and smaller pupil dilation.\nThe last study was designed to investigate the relationship between information processing and energy dissipation in the brain by quantifying the cerebral metabolic rate of oxygen (CMRO2) during a response to stimulus task in  fMRI (BOLD-ASL sequence). Hick-Hyman task maps a different number of stimuli to their response buttons\, depending on the complexity (entropy) of the trial or block. As a linear relationship exists between the quantity of  information processed (entropy) and the performance (response time) during the task\, we hypothesized that there should be a similar relation between the quantity of information needed to accomplish a task and the energy  allocated to do so. We addressed multiple technical issues related to CMRO2 computation in a cognitive task context. While we have improved and automatized the data analysis pipeline\, we faced significant challenges that  prevented us to reach a final conclusion on our initial hypothesis. \nKeywords: cognitive effort\, information theory\, visuo-motor tracking\, implicit learning\, CBF\, fMRI\, CMRO2 \nPublication\nAn information-theoretic measure of prediction during implicit learning of a quasi-sequential visuomotor tracking task \nJury\n\nPr. Julie Duqué (UCLouvain\, Bruxelles)\nPr. María Asunción Fernández Seara (Université de Navarre\, Pampelune)\nPr. Emmanuel Barbier (Institut de Neurosciences de Grenoble)\, Dr. Matthew Chalk (Institut de la vision\, Paris)\nDr. Gaël Jobard (Université de Bordeaux).\n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-simon-boylan/
CATEGORIES:iNCIA,Thesis
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