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自助餐厅饮食通过小胶质细胞激活诱导伏隔核的神经可塑性改变。

Cafeteria diet induces neuroplastic modifications in the nucleus accumbens mediated by microglia activation.

机构信息

Laboratory of Neuropharmacology (DCEXS), Parc de Recerca Biomèdica de Barcelona/Universitat Pompeu Fabra (PRBB/UPF), Spain.

Pathophysiology of Synaptic Transmission Laboratory, Institut de Génomique Fonctionnelle, France.

出版信息

Addict Biol. 2018 Mar;23(2):735-749. doi: 10.1111/adb.12541. Epub 2017 Sep 5.

DOI:10.1111/adb.12541
PMID:28872733
Abstract

High-palatable and caloric foods are widely overconsumed due to hedonic mechanisms that prevail over caloric necessities leading to overeating and overweight. The nucleus accumbens (NAc) is a key brain area modulating the reinforcing effects of palatable foods and is crucially involved in the development of eating disorders. We describe that prolonged exposure to high-caloric chocolate cafeteria diet leads to overeating and overweight in mice. NAc functionality was altered in these mice, presenting structural plasticity modifications in medium spiny neurons, increased expression of neuroinflammatory factors and activated microglia, and abnormal responses after amphetamine-induced hyperlocomotion. Chronic inactivation of microglia normalized these neurobiological and behavioural alterations exclusively in mice exposed to cafeteria diet. Our data suggest that prolonged exposure to cafeteria diet produces neuroplastic and functional changes in the NAc that can modify feeding behaviour. Microglia activation and neuroinflammation play an important role in the development of these neurobiological alterations.

摘要

由于愉悦机制占主导地位,超过了热量需求,导致过度饮食和超重,高美味和高热量的食物被广泛过度消费。伏隔核(NAc)是调节美味食物强化作用的关键大脑区域,对饮食失调的发展至关重要。我们描述了长时间暴露于高热量巧克力自助餐厅饮食会导致小鼠过度进食和超重。这些小鼠的 NAc 功能发生改变,表现出中脑多巴胺神经元结构可塑性改变,神经炎症因子表达增加,小胶质细胞激活,以及安非他命诱导的过度活跃后的异常反应。小胶质细胞的慢性失活仅在暴露于自助餐厅饮食的小鼠中使这些神经生物学和行为改变正常化。我们的数据表明,长时间暴露于自助餐厅饮食会导致 NAc 产生神经可塑性和功能变化,从而改变进食行为。小胶质细胞激活和神经炎症在这些神经生物学改变的发展中起着重要作用。

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