Noya Sara B, Sengupta Arjun, Yue Zhifeng, Weljie Aalim, Sehgal Amita
Howard Hughes Medical Institute, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Chronobiology and Sleep Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Eur J Neurosci. 2024 Dec;60(11):6605-6616. doi: 10.1111/ejn.16588. Epub 2024 Nov 14.
Sickness sleep and rebound following sleep deprivation share humoral signals including the rise of cytokines, in particular interleukins. Nevertheless, they represent unique physiological states with unique brain firing patterns and involvement of specific circuitry. Here, we performed untargeted metabolomics of mouse cortex and hippocampus to uncover changes with sickness and rebound sleep as compared with normal daily sleep. We found that the three settings are biochemically unique with larger differences in the cortex than in the hippocampus. Both sickness and rebound sleep shared an increase in tryptophan. Surprisingly, these two sleep conditions showed opposite modulation of the methionine-homocysteine cycle and differences in terms of the energetic signature, with sickness impinging on glycolysis intermediates whilst rebound increased the triphosphorylated form of nucleotides. These findings indicate that rebound following sleep deprivation stimulates an energy rich setting in the brain that is devoid during sickness sleep.
疾病、睡眠及睡眠剥夺后的反弹均共享体液信号，包括细胞因子尤其是白细胞介素水平的升高。然而，它们代表着独特的生理状态，具有独特的脑电活动模式并涉及特定的神经回路。在此，我们对小鼠皮层和海马进行了非靶向代谢组学分析，以揭示与正常日常睡眠相比，疾病状态及反弹睡眠时的变化。我们发现，这三种状态在生化层面具有独特性，皮层中的差异比海马中的更大。疾病状态和反弹睡眠时色氨酸均增加。令人惊讶的是，这两种睡眠状态在蛋氨酸-同型半胱氨酸循环上呈现相反的调节，且在能量特征方面存在差异，疾病状态影响糖酵解中间产物，而反弹睡眠则增加了核苷酸的三磷酸化形式。这些发现表明，睡眠剥夺后的反弹会刺激大脑进入一种在疾病睡眠期间缺乏的富含能量的状态。
