Department of Medicine, Central Clinical School, Monash University, Prahran, Victoria, 3004, Australia.
ToolGen, Inc., #1204, Byucksan Digital Valley 6-cha, Seoul, South Korea.
Sci Rep. 2017 Aug 21;7(1):8958. doi: 10.1038/s41598-017-09405-9.
Axo-glial units are highly organised microstructures propagating saltatory conduction and are disrupted during multiple sclerosis (MS). Nogo receptor 1 (NgR1) has been suggested to govern axonal damage during the progression of disease in the MS-like mouse model, experimental autoimmune encephalomyelitis (EAE). Here we have identified that adult ngr1 mice, previously used in EAE and spinal cord injury experiments, display elongated paranodes, and nodes of Ranvier. Unstructured paranodal regions in ngr1 mice are matched with more distributed expression pattern of Caspr. Compound action potentials of optic nerves and spinal cords from naïve ngr1 mice are delayed and reduced. Molecular interaction studies revealed enhanced Caspr cleavage. Our data suggest that NgR1 may regulate axo-myelin ultrastructure through Caspr-mediated adhesion, regulating the electrophysiological signature of myelinated axons of central nervous system (CNS).
轴-胶质单位是高度组织化的微观结构，可传播跳跃传导，并且在多发性硬化症 (MS) 期间被破坏。神经生长抑制因子受体 1 (NgR1) 已被提出在 MS 样小鼠模型、实验性自身免疫性脑脊髓炎 (EAE) 中控制疾病进展期间的轴突损伤。在这里，我们已经确定先前用于 EAE 和脊髓损伤实验的成年 ngr1 小鼠显示出伸长的连接部和郎飞结。ngr1 小鼠未结构化的连接部区域与 Caspr 的分布表达模式相匹配。来自幼稚 ngr1 小鼠的视神经和脊髓的复合动作电位延迟和减少。分子相互作用研究显示 Caspr 切割增强。我们的数据表明，NgR1 可能通过 Caspr 介导的黏附调节轴突-髓鞘超微结构，调节中枢神经系统 (CNS) 有髓轴突的电生理特征。
