To enable rapid propagation of action potentials, axons are ensheathed by myelin, a multilayered insulating membrane formed by oligodendrocytes. Most of the myelin is generated early in development, resulting in the generation of long-lasting stable membrane structures. Here, we explored structural and dynamic changes in central nervous system myelin during development. To achieve this, we performed an ultrastructural analysis of mouse optic nerves by serial block face scanning electron microscopy (SBF-SEM) and confocal time-lapse imaging in the zebrafish spinal cord. We found that myelin undergoes extensive ultrastructural changes during early postnatal development. Myelin degeneration profiles were engulfed and phagocytosed by microglia using exposed phosphatidylserine as one “eat me” signal. In contrast, retractions of entire myelin sheaths occurred independently of microglia and involved uptake of myelin by the oligodendrocyte itself. Our findings show that the generation of myelin early in development is an inaccurate process associated with aberrant ultrastructural features that require substantial refinement.

中文翻译：

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髓鞘形成产生异常的超微结构，由小胶质细胞解决

为了使动作电位能够快速传播，轴突被髓磷脂包裹，髓磷脂是一种由少突胶质细胞形成的多层绝缘膜。大多数髓磷脂是在发育早期产生的，从而产生持久稳定的膜结构。在这里，我们探索了中枢神经系统髓磷脂在发育过程中的结构和动态变化。为了实现这一目标，我们通过串行块面扫描电子显微镜 (SBF-SEM) 和斑马鱼脊髓的共焦延时成像对小鼠视神经进行超微结构分析。我们发现髓磷脂在出生后早期发育过程中经历了广泛的超微结构变化。使用暴露的磷脂酰丝氨酸作为“吃我”信号，小胶质细胞吞噬并吞噬髓磷脂变性。相反，整个髓鞘的收缩独立于小胶质细胞发生，并且涉及少突胶质细胞本身对髓磷脂的摄取。我们的研究结果表明，发育早期髓磷脂的生成是一个不准确的过程，与需要大量改进的异常超微结构特征相关。