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RESEARCH PRODUCT
Causal Link between n-3 Polyunsaturated Fatty Acid Deficiency and Motivation Deficits
Olivier BerdeauxElodie MassonStéphane GrégoireRoman WalleVéronique De Smedt-peyrusseLucy MartineFrank AbyClémentine Bosch-boujuBaptiste CaraballoSuzanne Van Der VeldtDavid W.l. MaXavier FioramontiJean-christophe HelblingJing X. KangSophie LayéGabriel Barreda-gómezPierre TrifilieffSylvie VancasselStéphanie CabaretGuillaume FerreiraMarie-lou BoyerTarson Tolentino-cortezFabien DucrocqAsma OummadiAndrea Continisubject
Male0301 basic medicineN-3 PUFAPhysiology[SDV]Life Sciences [q-bio]DopamineMice TransgenicNucleus accumbensMedium spiny neuronMice03 medical and health sciences0302 clinical medicineDopamineDopamine receptor D2Fatty Acids Omega-3medicineAnimalsMolecular BiologyPathological030304 developmental biologyNeuronsMedium spiny neuronschemistry.chemical_classification[SDV.GEN]Life Sciences [q-bio]/Genetics0303 health sciencesMotivationReceptors Dopamine D2business.industry[SCCO.NEUR]Cognitive science/NeuroscienceCell BiologyMice Inbred C57BLElectrophysiology[SDV.GEN.GA]Life Sciences [q-bio]/Genetics/Animal geneticsElectrophysiology030104 developmental biologychemistryNucleus accumbensFemalePolyunsaturated fatty acids[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Causal linkbusinessNeuroscience030217 neurology & neurosurgerymedicine.drugPolyunsaturated fatty aciddescription
International audience; Reward-processing impairment is a common symptomatic dimension of several psychiatric disorders. However, whether the underlying pathological mechanisms are common is unknown. Herein, we asked if the decrease in the n-3 polyunsaturated fatty acid (PUFA) lipid species, consistently described in these pathologies, could underlie reward-processing deficits. We show that reduced n-3 PUFA biostatus in mice leads to selective motivational impairments. Electrophysiological recordings revealed increased collateral inhibition of dopamine D2 receptor-expressing medium spiny neurons (D2-MSNs) onto dopamine D1 receptor-expressing MSNs in the nucleus accumbens, a main brain region for the modulation of motivation. Strikingly, transgenically preventing n-3 PUFA deficiency selectively in D2-expressing neurons normalizes MSN collateral inhibition and enhances motivation. These results constitute the first demonstration of a causal link between a behavioral deficit and n-3 PUFA decrease in a discrete neuronal population and suggest that lower n-3 PUFA biostatus in psychopathologies could participate in the etiology of reward-related symptoms.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2020-04-01 | Cell Metabolism |