Oligodendrocytes and Schwann cells are highly specialized glial cells that wrap axons with a multilayered myelin membrane for rapid impulse conduction. Investigators have recently identified axonal signals that recruit myelin-forming Schwann cells from an alternate fate of simple axonal engulfment. This is the evolutionary oldest form of axon-glia interaction, and its function is unknown. Recent observations suggest that oligodendrocytes and Schwann cells not only myelinate axons but also maintain their long-term functional integrity. Mutations in the mouse reveal that axonal support by oligodendrocytes is independent of myelin assembly. The underlying mechanisms are still poorly understood; we do know that to maintain axonal integrity, mammalian myelin-forming cells require the expression of some glia-specific proteins, including CNP, PLP, and MAG, as well as intact peroxisomes, none of which is necessary for myelin assembly. Loss of glial support causes progressive axon degeneration and possibly local inflammation, both of which are likely to contribute to a variety of neuronal diseases in the central and peripheral nervous systems.

中文翻译：

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轴突胶质信号和轴突功能的神经胶质支持。

少突胶质细胞和雪旺氏细胞是高度专门化的神经胶质细胞，它们用多层髓鞘膜包裹轴突，以实现快速脉冲传导。研究人员最近发现了轴突信号，该信号从简单轴突吞噬的另一种命运中募集形成髓磷脂的雪旺细胞。这是轴突-胶质细胞相互作用的进化最古老的形式，其功能尚不清楚。最近的观察表明，少突胶质细胞和雪旺氏细胞不仅具有髓鞘轴突，而且还保持其长期功能完整性。小鼠中的突变表明少突胶质细胞的轴突支持独立于髓磷脂组装。潜在的机制仍然知之甚少。我们确实知道要维持轴突的完整性，哺乳动物髓磷脂形成细胞需要表达某些神经胶质特异性蛋白，包括CNP，PLP，和MAG，以及完整的过氧化物酶体，髓鞘组装都不需要。失去神经胶质支持会导致进行性轴突变性，并可能引起局部炎症，这两者均可能导致中枢神经系统和周围神经系统的多种神经元疾病。