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X-WR-CALNAME:Bordeaux Neurocampus
X-ORIGINAL-URL:https://www.bordeaux-neurocampus.fr/en/
X-WR-CALDESC:Events for Bordeaux Neurocampus
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DTSTART:20231029T010000
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DTSTART;VALUE=DATE:20230916
DTEND;VALUE=DATE:20240617
DTSTAMP:20260529T202519
CREATED:20230831T131841Z
LAST-MODIFIED:20240529T183442Z
UID:162245-1694822400-1718582399@www.bordeaux-neurocampus.fr
SUMMARY:Exposition : Cervorama
DESCRIPTION:Agitez vos neurones ! \nA travers cette exposition\, Cap Sciences propose aux visiteurs de découvrir le cerveau sous toutes ses formes lors d’une visite ponctuée de manipulations\, de jeux et d’expériences… Ils pourront notamment explorer les mondes des cerveaux de l’escargot\, l’abeille\, le singe et l’homme\, tester leur mémoire dans le “cognitilab”\, découvrir leur cerveau en 3D grâce au cervomaton ou encore analyser les capacités des animaux ! \nUne exposition conçue et réalisée par Cap Sciences en partenariat avec Bordeaux Neurocampus\n \nEn savoir plus\nSite web : https://www.cap-sciences.net/au-programme/exposition/grand-public/cervorama/ \n
URL:https://www.bordeaux-neurocampus.fr/en/event/exposition-cervorama/
CATEGORIES:Events for all,not-calendar,pour tous homepage,Semaine du cerveau 2024
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20231002T080000
DTEND;TZID=Europe/Paris:20231006T170000
DTSTAMP:20260529T202519
CREATED:20230921T091823Z
LAST-MODIFIED:20230921T092233Z
UID:162544-1696233600-1696611600@www.bordeaux-neurocampus.fr
SUMMARY:Semaine Défi Mobilité des Comités Transitions de Bordeaux Neurocampus
DESCRIPTION:To get the new school year off to a good start\, the Transition Committees from the Bordeaux Neurocampus institutes are launching the Mobility Challenge Week! 🚲 \n🎯The aim? To challenge people’s commuting habits and move towards more environmentally-friendly solutions. \n🤔How? Car-sharing\, public transport\, cycling\, scootering\, walking\, etc. \n📅When? From Monday 1 to Friday 6 October 2023 \n🎁What’s in it for me? An assessment of your actions and gifts (during a friendly event: Tuesday 10 October). \nWhat is Mobility Challenge Week? 👟🌱 \n\nChange your home-work commuting habits towards more eco-responsible solutions during your working days (01/10 to 06/10)\nTuesday 10/10: compare the greenhouse gas emissions of a week’s worth of typical journeys with those made during this week’s challenge using the GDR Labo1point5 tool (https://labos1point5.org/commutes-simulator)\nComplete the survey that we will send you on Tuesday 10/10 to report on your efforts this week.\nTuesday 10 October from 13:00 to 14:00: Share and exchange ideas during a convivial moment and\, of course\, pick up your gift.\n\nCarpoolers\, get out your best jokes; tram users\, draw your season tickets; cyclists\, warm up your calves; scooterists\, oil your ball bearings; pedestrians\, wax your soles! \n
URL:https://www.bordeaux-neurocampus.fr/en/event/semaine-defi-mobilite-des-comites-transitions-de-bordeaux-neurocampus/
CATEGORIES:Transitions and well-being
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BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20231006T113000
DTEND;TZID=Europe/Paris:20231006T113000
DTSTAMP:20260529T202519
CREATED:20220917T122227Z
LAST-MODIFIED:20231002T084632Z
UID:150949-1696591800-1696591800@www.bordeaux-neurocampus.fr
SUMMARY:Monthly conference (PhD seminar) - Scott Kanoski
DESCRIPTION:Venue: Centre Broca \n\nScott KANOSKI\nUniversity of Southern California – USA\nhttps://kanoskilab.com/ \nInvited by Alice Fermigier (Ferreira and Trifilieff’s team – NutriNeuro) \nTitle\nA memo from your gut: cholinergic modulation of the gut-hippocampus axis \nAbstract\nVarious endocrine\, neuropeptide\, and neural signals regulate appetite\, meal size\, and satiety. Emerging evidence reveals that in addition to influencing food intake control\, these energy status-related biological systems also play a critical role in learning and memory function\, particularly with regards to remembering meal-associated episodic experiences and visuospatial information relevant for foraging behavior. Emerging findings identify the hippocampus as a critical brain region interfacing eating-relevant biological signals with learning and memory. Hippocampal neurons express receptors for multiple neuropeptides and circulating hormones associated with energy balance control\, and modulation of these receptors potently influences both appetitive (e.g.\, responsivity to environmental food cues) and consummatory (e.g.\, meal size control) behaviors. In addition to peptide systems\, we’ve recently identified a neural pathway through which within-meal physiological satiation signals engage hippocampal neurons to influence learning and memory. The vagus nerve\, which is a principal conduit of gut-brain satiation signaling\, communicates to hippocampal neurons through a multisynaptic pathway that includes the medial septum as a critical relay. This communication is functionally relevant to hippocampal-dependent memory function and is modulated by the gut-derived hormone\, ghrelin\, through its action on vagal afferent neurons. Our ongoing research is exploring the neural mechanisms orchestrating this newly identified gut-to-hippocampus axis\, with a recent focus on septal acetylcholine signaling as a critical interface between vagal and dietary influences on hippocampal function. Collective results are identifying neurobiological mechanisms mediating the bidirectional relationship between memory and eating behavior. \nBiosketch\nDr. Kanoski’s research focuses on the neurobiological control of food intake and body weight regulation. More specifically his laboratory focuses on understanding how the brain processes peripherally- and centrally-derived hormonal signals to control learned and motivated aspects of feeding behavior\, as well as to examine how these neuroendocrine signaling systems contribute to and are compromised by obesity and related metabolic disorders. At the center of this research is the hippocampus; a brain region traditionally linked with memory function\, but more recently shown to control higher-order aspects of feeding behavior. The lab also focuses on exploring the relationship between consuming saturated fatty acids and refined carbohydrates (i.e.\, “Western diets”) and the development of hippocampal dysfunction\, cognitive impairment\, and Alzheimer’s pathology. \n  \n  \n  \n\nPhD seminars are organized by the NBA\, Bordeaux Neurocampus\, and the Bordeaux Neurocampus Graduate Program \n
URL:https://www.bordeaux-neurocampus.fr/en/event/monthly-conference-phd-seminar-kanoski-scott/
CATEGORIES:For scientists,home-event,Monthly conferences
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DTSTART;TZID=Europe/Paris:20231006T140000
DTEND;TZID=Europe/Paris:20231006T140000
DTSTAMP:20260529T202519
CREATED:20230707T071011Z
LAST-MODIFIED:20231003T133526Z
UID:161155-1696600800-1696600800@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense -Anna Petitbon
DESCRIPTION:Venue : Centre Broca \nThesis defense in french \n\nAnna Petitbon\nTeam : Food Circus (NutriNeuro)\nThesis directed by : Pierre TRIFILIEFF \n\nTitle\nImplication of mesocorticolimbic dopamine transmission in behavioral flexibility: a role for dopamine and glutamate NMDA receptor heteromers \nAbstract\nThroughout their life\, nearly one in three people will be affected by a psychiatric disorder. However\, conventional pharmacological treatments remain relatively ineffective\, and are often accompanied by significant side effects due to their lack of selectivity. Therefore\, a consensus is emerging on the need to identify mechanisms underlying symptomatic dimensions common to several psychiatric pathologies (transnosographic approach); in order to develop personalized medicine in psychiatry. In this context\, executive function disorders – the cognitive processes that enable an individual to adapt to a constantly changing environment – are a common symptom of many psychiatric pathologies. Such symptoms are correlated with impaired dopaminergic transmission within the medial prefrontal cortex (mPFC) forming the mesocortical pathway\, and subcortical areas such as the ventral striatum or nucleus accumbens (NAc) forming the mesolimbic pathway. However\, the mechanisms by which this mesocorticolimbic dopaminergic transmission enables an individual to flexibly adapt his or her behavior remain unclear. Moreover\, in both structures\, the activity of dopaminoceptive neurons is strongly regulated by the convergence of glutamatergic and dopaminergic afferents. However\, how neurons integrate these signals is still poorly characterized. My preclinical thesis project therefore aims at unraveling how of mesocorticolimbic dopaminergic projections modulates behavioral flexibility\, and more specifically to establish the role of the physical interaction – or heteromerization – between D1 dopaminergic receptors (D1R) or D2 (D2R) and N-methyl-d-aspartate glutamatergic receptors (NMDA) within the mPFC and NAc. We show that this dopaminergic pathway is crucial for the animal’s ability to adapt to changes in the consequences of its actions. From a mechanistic point of view\, we demonstrate that D1/NMDA and D2/NMDA receptor heteromers in the mPFC and NAc constitute a central mechanism for mediating the effects of dopamine on executive functions. Indeed\, our results show that inhibiting mesocorticolimbic dopaminergic transmission through chemogenetic manipulation\, or blocking the ability of dopaminergic and NMDA receptors to form heteromers in NAc or mPFC through the use of interfering peptides\, specifically disrupts the ability of animals to update associations between lever pressing and reward\, in tasks assessing behavioral flexibility. These results suggest that mesocorticolimbic dopaminergic transmission is selectively involved in updating associations between an action and its consequences\, and that such effects are largely mediated by dopaminergic and NMDA receptor heteromers. Since these heteromers have distinct effects from their individual receptors\, these data suggest that they could be prime targets for the development of more specific therapeutic treatments: their specific manipulation could allow avoiding the side effects associated with conventional pharmacological treatments that target the cognate receptors. Using a calcium sensor approach coupled with fiber photometry\, we characterized i) the neural signature of mPFC dopaminoceptive neurons expressing D1R or D2R during Pavlovian and then operant conditioning\, especially during the update of associations\, and ii) the effect of heteromer blockade on these activities. We were able to demonstrate the presence of activity peaks at the time of reinforced lever pressing and of cues predicting the reward delivery\, as well as a decrease in activity during reward consumption\, and some of these signals are modulated by the D1/NMDA and D2/NMDA heteromers. This mechanism provides a better understanding of how behavioral adaptation processes are set in motion\, and thus constitutes an innovative therapeutic target. It could lead to the development of personalized treatments targeting executive function disorders and\, more specifically\, alterations in behavioral flexibility. \nKeywords: Behavioral flexibility – Dopamine – Glutamate – Receptor Heteromers – mPFC – NAc \nJury\nDr TRIFILIEFF Pierre\, Research director\, INRAE\, Bordeaux Thesis Director \nDr FAURE Philippe\, Research director\, CNRS\, Paris Reporter \nDr BURGUIERE Éric\, Research fellow\, CNRS\, Paris Reporter \nDr PARKES Shauna\, Research fellow\, CNRS\, Bordeaux Examinator \nDr FINO Élodie\, Research fellow\, CNRS\, Marseille Examinator \nDr GROC Laurent\, Research director\, CNRS\, Bordeaux Examinator \nDr VANHOUTTE Peter\, Research director\, CNRS\, Paris Invited \n\n
URL:https://www.bordeaux-neurocampus.fr/en/event/soutenance-de-these-anna-petitbon/
CATEGORIES:Thesis
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