Joost Sarah, Schweiger Felix, Pfeiffer Friederike, Ertl Carolin, Keiler Jonas, Frank Marcus, Kipp Markus
Institute of Anatomy, Rostock University Medical Center, Rostock, Germany.
Werner Reichardt Centre for Integrative Neuroscience, University of Tübingen, Tübingen, Germany.
Front Cell Neurosci. 2022 Feb 18;16:709596. doi: 10.3389/fncel.2022.709596. eCollection 2022.
Myelin damage is a histopathological hallmark of multiple sclerosis lesions. Results of studies suggest that impaired myelin-axon interaction characterized by focal myelin detachments is an early event during lesion genesis. In this study, we investigated the ultrastructural changes of the axon-myelin interface in the cuprizone model using serial block face scanning electron microscopy and immunohistochemistry. We show that non-inflammatory injury of oligodendrocytes by cuprizone intoxication results in myelin vacuole formation and axonal swellings, paralleled by early alterations of the node of Ranvier cytoarchitecture. This remarkable resemblance of ultrastructural myelin characteristics in multiple sclerosis and the cuprizone animal model suggests that the cuprizone model is a valuable tool to study early pathologies during lesion formation.
髓鞘损伤是多发性硬化症病变的组织病理学标志。研究结果表明，以局灶性髓鞘脱离为特征的髓鞘 - 轴突相互作用受损是病变发生过程中的早期事件。在本研究中，我们使用连续块面扫描电子显微镜和免疫组织化学方法，研究了在 cuprizone 模型中轴突 - 髓鞘界面的超微结构变化。我们发现，cuprizone 中毒导致少突胶质细胞的非炎性损伤，进而引起髓鞘空泡形成和轴突肿胀，同时伴有郎飞结细胞结构的早期改变。多发性硬化症和 cuprizone 动物模型中超微结构髓鞘特征的显著相似性表明，cuprizone 模型是研究病变形成过程中早期病理变化的有价值工具。
