Metabolism and redox signalling share critical nodes in the nervous system. In the last years, a series of major findings have challenged the current vision on how neural reactive oxygen species (ROS) are produced and handled in the nervous system. Once regarded as deleterious by-products, ROS are now shown to be essential for a metabolic and redox crosstalk. In turn, this coupling defines neural viability and function to control behaviour or leading to neurodegeneration when compromised. Findings like a different assembly of mitochondrial respiratory supercomplexes in neurons and astrocytes stands behind a divergent production of ROS in either cell type, more prominent in astrocytes. ROS levels are however tightly controlled by an antioxidant machinery in astrocytes, assumed as more efficient than that of neurons, to regulate redox signalling. By exerting this control in ROS abundance, metabolic functions are finely tuned in both neural cells. Further, a higher engagement of mitochondrial respiration and oxidative function in neurons, underpinned by redox equivalents supplied from the pentose phosphate pathway and from glia, differs from the otherwise strong glycolytic capacity of astrocytes. Here, we recapitulate major findings on how ROS and metabolism differ between neural cells but merge to define reciprocal signalling pathways, ultimately defining neural function and fate.

中文翻译：

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神经元-星形胶质细胞界面上相互交织的 ROS 和代谢信号。

代谢和氧化还原信号共享神经系统中的关键节点。在过去几年中，一系列重大发现挑战了当前关于神经系统中如何产生和处理神经活性氧 (ROS) 的观点。曾经被视为有害副产品的 ROS 现在被证明对于代谢和氧化还原串扰至关重要。反过来，这种耦合定义了神经活力和功能，以控制行为或在受到损害时导致神经退化。神经元和星形胶质细胞中线粒体呼吸超级复合物的不同组装等发现支持两种细胞类型中不同的 ROS 产生，在星形胶质细胞中更为突出。然而，ROS 水平受到星形胶质细胞中抗氧化机制的严格控制，被认为比神经元更有效，以调节氧化还原信号。通过对 ROS 丰度施加这种控制，两个神经细胞的代谢功能都得到了微调。此外，由磷酸戊糖途径和神经胶质提供的氧化还原当量支持的神经元中线粒体呼吸和氧化功能的更高参与，不同于星形胶质细胞的其他强糖酵解能力。在这里，我们概括了关于神经细胞之间 ROS 和代谢如何不同但合并以定义相互信号通路，最终定义神经功能和命运的主要发现。不同于星形胶质细胞的强糖酵解能力。在这里，我们概括了关于神经细胞之间 ROS 和代谢如何不同但合并以定义相互信号通路，最终定义神经功能和命运的主要发现。不同于星形胶质细胞的强糖酵解能力。在这里，我们概括了关于 ROS 和代谢如何在神经细胞之间不同但合并以定义相互信号通路，最终定义神经功能和命运的主要发现。