Sleep deprivation (SD) is a common feature in modern society. Prolonged sleep deprivation causes cognition deficits and depression-like behavior in the model of animal experiments. Endocannabinoid system are key modulators of synaptic function, which were related to memory and mood. Although the underlying mechanism remains unknown, several studies indicated the benefits of polyunsaturated fatty acids (PUFAs, linolenic acid, 39.7 %; linoleic acid, 28 %; and oleic acid, 22 %) on brain function through the endocannabinoid system. The present study aimed to evaluate the influence of dietary PUFAs on cognition deficits induced by sleep deprivation in Sprague Dawley rats. The rats were sleep deprivation continuously for 7 days and fed with PUFAs at three different dosages (2, 4 and 8 μl/g body weight) at the meantime. The effect of PUFAs on cognition was investigated by object recognition test while depressive-like behavior were detected using sucrose preference test and forced swim test. The mechanism of PUFAs was elucidated by hippocampal synaptic transmission analyses. The resluts revealed that SD led to the disorder of cognition and mood which was improved by the supplement of PUFAs. SD significantly increased the mEPSC frequency, and decreased the protein level of cannabinoid type-1 receptors (CB1R). These changes were restored by supplement of PUFAs, which showed a similar level to the control group. Behaviour tests showed that the positive effects on repairing cognition and anxiety disorders were almost completely abolished when the CB1R receptor antagonist rimonabant was applied to the SD rats. These findings indicated that PUFAs are a factor regulating cognition deficits and depression induced by SD via cannabinoid type-1 receptors.

中文翻译：

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饮食中多不饱和脂肪酸的摄入通过睡眠剥夺大鼠的大麻素系统减轻了认知障碍和抑郁样行为。

睡眠剥夺（SD）是现代社会的普遍特征。在动物实验模型中，长时间的睡眠剥夺会导致认知缺陷和抑郁样行为。内源性大麻素系统是突触功能的关键调节剂，与记忆和情绪有关。尽管尚不清楚其基本机制，但多项研究表明，通过内源性大麻素系统，多不饱和脂肪酸（PUFA，亚麻酸为39.7％；亚油酸为28％；油酸为22％）对脑功能的益处。本研究旨在评估饮食中PUFA对Sprague Dawley大鼠睡眠剥夺所致认知功能障碍的影响。将大鼠连续剥夺睡眠7天，并同时以三种不同剂量（2、4和8μl/ g体重）喂食PUFA。通过对象识别测试研究了PUFA对认知的影响，同时使用蔗糖偏爱测试和强迫游泳测试检测了抑郁样行为。海马突触传递分析阐明了PUFAs的机制。结果表明，SD导致认知和情绪障碍，补充PUFA可以改善这种障碍。SD显着提高了mEPSC频率，并降低了大麻素1型受体（CB1R）的蛋白质水平。这些变化通过补充PUFA得以恢复，显示出与对照组相似的水平。行为测试表明，将CB1R受体拮抗剂利莫那班应用于SD大鼠后，对修复认知和焦虑症的积极作用几乎被完全消除。