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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.
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Contributor : Marion Desailly Connect in order to contact the contributor
Submitted on : Wednesday, April 22, 2020 - 10:38:21 AM
Last modification on : Friday, September 17, 2021 - 2:32:03 PM

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Fabien Ducrocq, Roman Walle, Andrea Contini, Asma Oummadi, Baptiste Caraballo, et al.. Causal link between n-3 polyunsaturated fatty acid deficiency and motivation deficits. Cell Metabolism, Elsevier, 2020, 31 (4), pp.755-772. ⟨10.1016/j.cmet.2020.02.012⟩. ⟨hal-02550371⟩



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