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Causal Link between n-3 Polyunsaturated Fatty Acid Deficiency and Motivation Deficits.

Abstract：

: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.

journal_name

Cell Metab

journal_title

Cell metabolism

authors

Ducrocq F,Walle R,Contini A,Oummadi A,Caraballo B,van der Veldt S,Boyer ML,Aby F,Tolentino-Cortez T,Helbling JC,Martine L,Grégoire S,Cabaret S,Vancassel S,Layé S,Kang JX,Fioramonti X,Berdeaux O,Barreda-Gómez G,Masso

doi

10.1016/j.cmet.2020.02.012

subject

Has Abstract

pub_date

2020-04-07 00:00:00

pages

755-772.e7

issue

4

eissn

1550-4131

issn

1932-7420

pii

S1550-4131(20)30071-1

journal_volume

31

pub_type

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