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在脊椎中枢神经系统中,少突胶质细胞能形成轴突的髓鞘。髓鞘对轴突具有保护作用,使轴突具有电绝缘的特性,其独特的节段状结构使髓鞘化的神经轴突能快速、跳跃式地传导神经冲动。髓鞘损伤常见于脊髓损伤和一些慢性神经退行性疾病,由其引起的轴突传导阻滞被认为是引起损伤相关的神经并发症的主要原因。钾离子通道在发生于脊髓损伤和多发性硬化征的轴突传导阻滞中扮演重要角色。髓鞘损伤后会暴露钾离子通道,引起钾离子泄漏,从而阻断神经传导。将钾离子通道阻滞后,离子泄漏得到抑制,进而能促进神经传导。本综述主要详细介绍了修复轴突神经传导功能技术的研究进展和脱髓鞘轴突的神经功能。最近的研究表明,4-氨基吡啶能有效治疗多发性硬化征。此外,转化型研究也筛选出了一些能有效修复轴突神经传导的新型的钾离子通道阻滞剂。
In the spinal central nervous system, oligodendrocytes form the myelinated axons. Myelin has a protective effect on the axon, so that the axon has the characteristics of electrical insulation, its unique segmental structure of myelinated axons can quickly and leapfrog conductive nerve impulses. Myelin damage, a common cause of spinal cord injury and a number of chronic neurodegenerative diseases, is thought to be the major cause of injury-related neurological complications. Potassium channels play an important role in axonal block in spinal cord injury and multiple sclerosis. Myelin injury exposes potassium channels, causing leakage of potassium ions, thereby blocking nerve conduction. After blocking the potassium channel, the ion leakage is inhibited, which in turn can promote nerve conduction. This review mainly introduces the research progress of repair axonal nerve conduction function and the neurological function of demyelinating axon. Recent studies have shown that 4-aminopyridine is effective in treating multiple sclerosis. In addition, the transformation study also screened out some new potassium channel blockers that can effectively repair axonal nerve conduction.