小柯机器人

近日，法国波尔多大学Pierre Trifilieff 和Fabien Ducrocq等合作发现n-3多不饱和脂肪酸缺乏与动力缺乏之间的因果关系。2020年3月5日，国际学术期刊《细胞-代谢》发表了这一成果。

研究人员猜想在这些病理学发现的n-3多不饱和脂肪酸（PUFA）类脂质的减少是否可能是奖励行为缺陷的基础。研究表明，减少小鼠n-3 PUFA的生物状态会导致选择性的动力障碍。

电生理学记录显示，伏隔核中多巴胺D2受体表达的中型多棘神经元（D2-MSNs）对表达多巴胺D1受体的MSNs侧支抑制增加，伏隔核是大脑主要调节动力的区域。特别是在表达D2的神经元中通过转基因方式选择性地阻止n-3 PUFA缺乏，可中和MSN侧支抑制并增强动力。

这些结果首次证明了行为缺陷与离散神经元人群中n-3 PUFA减少之间的因果关系，并表明心理病理学中较低的n-3 PUFA生物状态可能是奖赏相关症状的病因。

研究人员表示，奖励行为障碍是几种精神病的常见症状。但是，尚不清楚其潜在的病理机制是否一致。

附：英文原文

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

Author: Fabien Ducrocq, Roman Walle, Andrea Contini, Asma Oummadi, Baptiste Caraballo, Suzanne van der Veldt, Marie-Lou Boyer, Frank Aby, Tarson Tolentino-Cortez, Jean-Christophe Helbling, Lucy Martine, Stéphane Grégoire, Stéphanie Cabaret, Sylvie Vancassel, Sophie Layé, Jing Xuan Kang, Xavier Fioramonti, Olivier Berdeaux, Gabriel Barreda-Gómez, Elodie Masson, Guillaume Ferreira, David W.L. Ma, Clementine Bosch-Bouju, Véronique De Smedt-Peyrusse, Pierre Trifilieff

Issue&Volume: 2020-03-05

Abstract: Reward-processing impairment is a common symptomatic dimension of several psychiatricdisorders. However, whether the underlying pathological mechanisms are common is unknown.Herein, we asked if the decrease in the n-3 polyunsaturated fatty acid (PUFA) lipidspecies, consistently described in these pathologies, could underlie reward-processingdeficits. We show that reduced n-3 PUFA biostatus in mice leads to selective motivationalimpairments. Electrophysiological recordings revealed increased collateral inhibitionof dopamine D2 receptor-expressing medium spiny neurons (D2-MSNs) onto dopamine D1receptor-expressing MSNs in the nucleus accumbens, a main brain region for the modulationof motivation. Strikingly, transgenically preventing n-3 PUFA deficiency selectivelyin D2-expressing neurons normalizes MSN collateral inhibition and enhances motivation.These results constitute the first demonstration of a causal link between a behavioraldeficit and n-3 PUFA decrease in a discrete neuronal population and suggest that lowern-3 PUFA biostatus in psychopathologies could participate in the etiology of reward-relatedsymptoms.

DOI: 10.1016/j.cmet.2020.02.012

Source: https://www.cell.com/cell-metabolism/fulltext/S1550-4131(20)30071-1

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