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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:20260329T010000
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DTSTART;VALUE=DATE:20261109
DTEND;VALUE=DATE:20261111
DTSTAMP:20261006T154233
CREATED:20260914T130154Z
LAST-MODIFIED:20261001T140343Z
UID:206373-1794182400-1794355199@www.bordeaux-neurocampus.fr
SUMMARY:French Kinase Conference - 1st edition
DESCRIPTION:Venue: European Institute of Chemistry and Biology (IECB) \n\nThis conference aims to bring together the French community of biologists\, structural biologists\, and medicinal chemists sharing a common interest in protein kinases. \nThe program will include a keynote lecture by: \n\nDr. Dario Alessi (PPU\, Dundee\, UK)\, President of IUBMB\n\nAnd three invited speakers : \n\nDr. Julie Guillermet-Guibert (CRCT\, Toulouse\, Inserm/CNRS/UPS)\nDr. Matthew Bowler (EMBL\, Grenoble)\nDr. Laurent Meijer (ManRos Therapeutics & Perha Pharmaceuticals\, Roscoff)\n\nOral and poster presentations\nSelected based on abstract submissions. \n\nAbstract submission deadline: October 2nd (submission portal — login via Sciencesconf required)\nRegistration deadline: October 16th (registration portal)\n\nMore information\nhttps://fkc2026.sciencesconf.org/ \n
URL:https://www.bordeaux-neurocampus.fr/en/event/french-kinase-conference-1st-edition/
CATEGORIES:For scientists,home-event,Other events,Symposium
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DTSTART;TZID=Europe/Paris:20261109T143000
DTEND;TZID=Europe/Paris:20261109T143000
DTSTAMP:20261006T154233
CREATED:20260916T092827Z
LAST-MODIFIED:20260925T134544Z
UID:206032-1794234600-1794234600@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Kevin Letort
DESCRIPTION:Venue: BBS \nDefense in french \n\nKévin Letort \nDirected by : Karine Guillem \nTeams : Choice\, Addiction and Neurodysfunctions (Candy) \ntitle\nEscalation\, Relapse\, and Attention Deficits in a New Model of Nicotine Addiction in Rats: Role of Prefrontal’s Interneurons \nAbstract\nWith more than 1.3 billion smokers worldwide\, tobacco addiction\, whose main addictive substance is nicotine\, remains the most prevalent addiction and one of the leading causes of preventable death. Clinically\, the diagnosis of this disorder relies on a set of criteria\, among which the loss of control over consumption\, notably characterized by an escalation of drug intake\, plays a central role. However\, this phenomenon of nicotine intake escalation has long remained difficult to model in animals. \nTo overcome this limitation\, the laboratory recently developed an escalation model in rats\, based on intravenous self-administration of increasing doses of nicotine\, which induces escalated nicotine intake and heightened drug motivation compared to the standard model. The first part of this project consisted of evaluating the consequences of this escalation on two other key diagnostic criteria for addiction\, namely abstinence and relapse\, in male and female rats. This study demonstrated that rats having escalated their nicotine intake exhibit greater difficulty extinguishing drug-seeking behavior as well as increased vulnerability to nicotine-induced relapse\, with no sex differences. \nOn a neurobiological level\, drug intake and the control of drug seeking rely directly on the medial prefrontal cortex (mPFC)\, whose activity is finely regulated by local inhibitory interneurons. The second part of my work thus focused on the cellular consequences of this escalation on mPFC microcircuitry\, and the causal role of interneurons in this phenomenon. The results revealed that nicotine intake escalation induces coordinated cellular alterations in pyramidal neurons and specific interneuron sub-populations\, thereby fundamentally reshaping mPFC microcircuits. \nFinally\, while acute nicotine administration enhances attention\, chronic smokers have impaired mPFC function alongside marked attentional deficits during withdrawal. In the last part of this project\, we evaluated attentional performance during chronic intake and nicotine withdrawal\, while chemogenetically manipulating mPFC interneurons activity. Our results i) confirm the key role played by mPFC interneurons in the pro-cognitive effects of nicotine\, and ii) demonstrate that interneuron hyperactivity and abnormal gamma oscillations underlie the persistent attentional deficits observed during withdrawal following escalated nicotine intake. \nOverall\, this work reveals the complex role of prefrontal interneurons in the loss of control over nicotine intake and withdrawal-induced attentional deficits\, paving the way for more targeted treatments for smoking cessation. \nKey words\nNicotine\, Addiction\, Prefrontal Cortex\, Interneurons \nJury\nBESSON Morgane\, CR\, CNRS UMR 3571\, Institut pasteur Paris                                   Rapporteuse \nTHIRIET Nathalie\, PR\, INSERM UMR-S 1084\, Univ. Poitiers                                           Rapporteuse \nDEGOULET Michael\, CR\, CNRS UMR 7289\, Univ. Aix-Marseille                                   Examinateur \nGEORGES François\, DR\, CNRS UMR 5293\, Univ. Bordeaux                                            Examinateur \nDEROCHE – GAMONET Véronique\, DR\, INSERM UMR 1215\, Univ. Bordeaux       Examinatrice \nGUILLEM Karine\, DR\, CNRS UMR 5287\, Univ. Bordeaux                                                Directrice de thèse \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-kevin-letort/
CATEGORIES:Thesis
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