Muramatsu Rieko, Yamashita Toshihide
Department of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Osaka 565-0871, Japan; Japan Science and Technology Agency, Core Research for Evolutional Science and Technology, Chiyoda, Tokyo 102-0075, Japan.
Neurosci Res. 2014 Jan;78:45-9. doi: 10.1016/j.neures.2013.07.002. Epub 2013 Jul 26.
Damage to the central nervous system (CNS) leads to the disruption of the axonal network and causes neurological dysfunction. Recovery of neurological functions requires restoration of the axonal network; however, injured axons in the adult mammalian CNS rarely regenerate after injury. Failure of the injured axon to regenerate is attributed at least partly to the inhibitory molecules of the CNS: several proteins have been identified in the CNS that inhibit axonal regeneration. In addition, the molecular mechanisms underlying the manner via which these inhibitors prevent axonal regeneration have been clarified. The neutralization of nonpermissive substrate properties of the CNS has been shown to promote axonal regeneration in an animal model of CNS injury. Drugs that promote axonal regeneration, some of which have undergone clinical trials, have been developed by pharmaceutical companies. However, spontaneous functional recovery occurs sometimes after CNS injury. This review will describe the new concept of the molecular mechanism of restoration of the neuronal network, with a special focus on our recent reports.
中枢神经系统（CNS）损伤会导致轴突网络中断并引起神经功能障碍。神经功能的恢复需要轴突网络的重建；然而，成年哺乳动物中枢神经系统中的受损轴突在损伤后很少再生。受损轴突无法再生至少部分归因于中枢神经系统的抑制分子：中枢神经系统中已鉴定出几种抑制轴突再生的蛋白质。此外，这些抑制剂阻止轴突再生的分子机制也已阐明。在中枢神经系统损伤的动物模型中，已证明中和中枢神经系统的非允许底物特性可促进轴突再生。制药公司已开发出促进轴突再生的药物，其中一些已进入临床试验阶段。然而，中枢神经系统损伤后有时会出现自发的功能恢复。本综述将描述神经元网络恢复分子机制的新概念，特别关注我们最近的报告。
