| First Author | Ducrocq F | Year | 2020 |
| Journal | Cell Metab | Volume | 31 |
| Issue | 4 | Pages | 755-772.e7 |
| PubMed ID | 32142670 | Mgi Jnum | J:287742 |
| Mgi Id | MGI:6406616 | Doi | 10.1016/j.cmet.2020.02.012 |
| Citation | Ducrocq F, et al. (2020) Causal Link between n-3 Polyunsaturated Fatty Acid Deficiency and Motivation Deficits. Cell Metab 31(4):755-772.e7 |
| abstractText | 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. |
