近日，美国科罗拉多大学医学院Ethan G. Hughes及其研究小组发现，运动学习通过新生的和存活的少突胶质细胞促进髓鞘再生。2020年5月18日，《自然—神经科学》在线发表了这项成果。

研究人员发现，虽然学习前肢伸展任务会瞬时抑制少突胶质生成，但随后会增加少突胶质前体细胞的分化、少突胶质细胞的生成以及前肢运动皮层中髓鞘的重塑。脱髓鞘后，神经元立即表现出过度兴奋性，学习受到损害，并且行为干预对髓鞘再生没有益处。但是，部分髓鞘再生可恢复神经元和行为功能，从而可以通过学习来增强少突胶质生成、裸露的轴突的髓鞘再生成以及幸存的少突胶质细胞产生新髓鞘的能力。

虽然在以前是有争议的，研究人员表明成熟的少突胶质细胞不仅可以生成髓鞘，而且在脱髓鞘后还可以增加髓鞘的保护，从而为治疗提供了新的靶点。总之，这些发现表明，精确定时的运动学习可通过增强新生的以及存活的少突胶质细胞的髓鞘再生来改善脱髓鞘损伤的恢复。

据悉，神经疾病中少突胶质细胞的丧失使轴突容易受到损害和变性，而活动依赖性的髓鞘形成可能是一种改善损伤后髓鞘形成的内在机制。

附：英文原文

Title: Motor learning promotes remyelination via new and surviving oligodendrocytes

Author: Clara M. Bacmeister, Helena J. Barr, Crystal R. McClain, Michael A. Thornton, Dailey Nettles, Cristin G. Welle, Ethan G. Hughes

Issue&Volume: 2020-05-18

Abstract: Oligodendrocyte loss in neurological disease leaves axons vulnerable to damage and degeneration, and activity-dependent myelination may represent an endogenous mechanism to improve remyelination following injury. Here we report that, while learning a forelimb reach task transiently suppresses oligodendrogenesis, it subsequently increases oligodendrocyte precursor cell differentiation, oligodendrocyte generation and myelin sheath remodeling in the forelimb motor cortex. Immediately following demyelination, neurons exhibit hyperexcitability, learning is impaired and behavioral intervention provides no benefit to remyelination. However, partial remyelination restores neuronal and behavioral function, allowing learning to enhance oligodendrogenesis, remyelination of denuded axons and the ability of surviving oligodendrocytes to generate new myelin sheaths. Previously considered controversial, we show that sheath generation by mature oligodendrocytes is not only possible but also increases myelin pattern preservation following demyelination, thus presenting a new target for therapeutic interventions. Together, our findings demonstrate that precisely timed motor learning improves recovery from demyelinating injury via enhanced remyelination from new and surviving oligodendrocytes.

DOI: 10.1038/s41593-020-0637-3

Source: https://www.nature.com/articles/s41593-020-0637-3