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.

中文翻译：

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驱动轴突再生的轴突内机制。

外周和中枢神经系统的创伤性损伤通常会导致轴突切断术，其中轴突失去与其目标的连接，导致功能丧失。损伤部位远端的轴突节段与细胞体失去连接并退化。外围的轴突神经元可以自发地产生再生反应并重新连接到其去神经支配的目标组织，尽管这在人类中很少完成。相比之下，脊髓和大脑中的轴突切断术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，重点关注从支持再生生长的轴突开始的事件。我们将此与已知的中枢神经系统轴突损伤反应进行对比。