Causal Link between n-3 Polyunsaturated Fatty Acid Deficiency and Motivation Deficits
Langue
EN
Article de revue
Ce document a été publié dans
Cell Metabolism. 2019-01-01, vol. 31, n° 4, p. 755-772.e7
Résumé en anglais
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 ...Lire la suite >
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 Acids (PUFAs) 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 deficits. Electrophysiological recordings revealed increased collateral inhibition of dopamine D2 receptor (D2R)-expressing medium spiny neurons (iMSNs) onto dopamine D1 receptor-expressing (d)MSNs in the nucleus accumbens, a main brain region for the modulation of motivation. Strikingly, transgenically preventing n-3 PUFA deficiency selectively in D2R-expressing neurons normalizes MSNs 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 to the etiology of reward-related symptoms.< Réduire
Mots clés en anglais
Polyunsaturated fatty acids
Motivation
Dopamine
Nucleus accumbens
Medium spiny neurons
Electrophysiology
Unités de recherche