Department of Biological Sciences, University of South Carolina, Columbia, SC, USA.
Department of Biological Sciences, University of South Carolina, Columbia, SC, USA.
Brain Res. 2020 Aug 1;1740:146864. doi: 10.1016/j.brainres.2020.146864. Epub 2020 Apr 28.
Traumatic injury to the peripheral and central nervous systems very often causes axotomy, where an axon loses connections with its target resulting in loss of function. The axon segments distal to the injury site lose connection with the cell body and degenerate. Axotomized neurons in the periphery can spontaneously mount a regenerative response and reconnect to their denervated target tissues, though this is rarely complete in humans. In contrast, spontaneous regeneration rarely occurs after axotomy in the spinal cord and brain. Here, we concentrate on the mechanisms underlying this spontaneous regeneration in the peripheral nervous system, focusing on events initiated from the axon that support regenerative growth. We contrast this with what is known for axonal injury responses in the central nervous system. Considering the neuropathy focus of this special issue, we further draw parallels and distinctions between the injury-response mechanisms that initiate regenerative gene expression programs and those that are known to trigger axon degeneration.
周围和中枢神经系统的创伤性损伤常常导致轴突切断，其中轴突失去与靶标之间的连接，导致功能丧失。损伤部位远端的轴突段与细胞体失去连接并退化。外周的轴突切断神经元可以自发地启动再生反应并重新连接到去神经的靶组织，尽管在人类中很少完全恢复。相比之下，脊髓和大脑中的轴突切断后很少发生自发再生。在这里，我们专注于周围神经系统中这种自发再生的机制，重点关注支持再生生长的轴突启动的事件。我们将其与中枢神经系统中轴突损伤反应的已知情况进行对比。考虑到本期特刊的神经病变重点，我们进一步比较和区分了启动再生基因表达程序的损伤反应机制和已知触发轴突退化的机制。
