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:20250330T010000
END:DAYLIGHT
BEGIN:STANDARD
TZOFFSETFROM:+0200
TZOFFSETTO:+0100
TZNAME:CET
DTSTART:20251026T010000
END:STANDARD
END:VTIMEZONE
BEGIN:VEVENT
DTSTART;TZID=Europe/Paris:20250926T140000
DTEND;TZID=Europe/Paris:20250926T140000
DTSTAMP:20260306T183704
CREATED:20250313T161303Z
LAST-MODIFIED:20250901T152030Z
UID:181690-1758895200-1758895200@www.bordeaux-neurocampus.fr
SUMMARY:Thesis defense - Lola Hardt
DESCRIPTION:Venue: Centre Broca \nDefense in english \n\nTitle\nImplication of polyunsaturated fatty acid (PUFA) biostatus in dopamine transmission-related reward processing deficits \nRésumé\nReward processing deficits underly shared symptomatic dimension across psychiatric disorders such as schizophrenia\, bipolar disorder and major depression. These impairments are often linked to dysfunction of mesocorticolimbic dopaminergic pathway\, suggesting shared underlying mechanisms. Interestingly\, clinical studies have consistently described a decrease in n-3 polyunsaturated fatty acids (PUFA) in a subpopulation of patients with these disorders (Conklin et al.\, 2010; Messamore and McNamara\, 2016). Here we show that developmental n-3 PUFA deficiency leads to an imbalance in the mesocorticolimbic pathway with cortical hypodopaminergia and striatal hyperdopaminergia\, together with aberrant wiring of striatal dopamine terminals which relate to changes in gene networks involved in neuronal transmission and axon development in VTA DA neurons. Furthermore\, DA dynamics in relation with action reinforcement and reward prediction in the mPFC and the NAc\, respectively\, were found to be altered under n-3 PUFA deficiency\, potentially revealing reward processing deficits implicated in related impaired behaviors. Indeed\, n-3 PUFA deficiency while sparing learning and flexible expression of action-outcome associations\, leads to motivational deficits and increased choice impulsivity. Importantly\, transgenic normalization of PUFA biostatus in DA neurons specifically was sufficient to prevent behavioral deficits\, demonstrating the causal link between developmental n-3 PUFA deficiency\, mesocorticolimbic imbalance and reward processing deficits\, relevant to psychiatric disorders. By elucidating  shared pathological mechanisms across diagnostic boundaries\, this work might unravel neurodevelopmental and circuit level vulnerabilities under n-3 PUFA deficiency which could pave the way for early interventions\, preventive strategies\, and more personalized approaches to treatment in psychiatry with PUFA biostatus as a clinically relevant biomarker. \nKeywords: Psychiatric Disorders\, n-3 PUFA Deficiency\, Reward Processing Deficits\, Dopamine \n  \nPublications\nRoman Walle\, Anna Petitbon\, Giulia R. Fois\, Christophe Varin\, Enrica Montalban\, Lola Hardt\, Andrea Contini\, Maria Florencia Angelo\, Mylène Potier\, Rodrigue Ortole\, Asma Oummadi\, Véronique De Smedt-Peyrusse\, Roger A Adan\, Bruno Giros\, Francis Chaouloff\, Guillaume Ferreira\, Alban de Kerchove d’Exaerde\, Fabien Ducrocq\, François Georges\, Pierre Trifilieff.\nNucleus accumbens D1- and D2-expressing neurons control the balance between feeding and activity-mediated energy expenditure (2023)\ndoi: https://doi.org/10.1101/2022.05.05.490599 \nAlessia Costa\, Eva Ducourneau\, Lorenzo Curti\, Alessio Masi\, Guido Mannaioni\, Lola Hardt\, Essi F Biyong\, Mylène Potier\, Patrizio Blandina\, Pierre Trifilieff\, Gustavo Provensi\, Guillaume Ferreira\, M Beatrice Passani\nChemogenetic activation or inhibition of histaminergic neurons bidirectionally modulates recognition memory formation and retrieval in male and female mice (2023)\ndoi: https://doi.org/10.21203/rs.3.rs-3714805/v1 \nJury\nDr BELUJON Pauline\, Maîtresse de conférences\, Laboratoire de Neurosciences Expérimentales et Cliniques\, Rapporteure\nDr GEORGES François\, Directeur de recherche\, Insitut de Maladies Neurodégénérative\, CNRS UMR 5293\, Invité\nDr TRIFILIEFF Pierre\, Directeur de recherche\, Laboratoire NutriNeurO\, UMR INRAE 1286\, Directeur de Thèse\nDr CARNICELLA Sébastien\, Directeur de recherche\, Grenoble Institut des Neurosciences\, Inserm U1216\, Université Grenoble Alpes\, Rapporteur\nDr VALJENT Emmanuel\, Directeur de recherche\, Institute For Neurosciences Of Montpellier\, Examinateur\nDr FLORES Cecilia\, Full professor\, The Douglas Research Centre\, Examinatrice \n
URL:https://www.bordeaux-neurocampus.fr/en/event/thesis-defense-lola-hardt/
CATEGORIES:Nutrineuro,Thesis
END:VEVENT
END:VCALENDAR