Molecular mechanism of regeneration and plasticity of the injured central nervous system

在成年哺乳动物中枢神经系统（CNS）中，损伤的轴突表现出非常有限的再生能力是众所周知的。由于缺乏适当的轴突再生，对成人大脑和脊髓的创伤性损伤经常导致永久性神经元缺陷，如瘫痪。已经在髓磷脂中鉴定了CNS中的几种轴突生长抑制剂。这些蛋白质导致受损CNS的再生缺乏。然而，值得注意的是，自发的功能恢复有时发生在CNS损伤之后。预先存在的通路中的突触可塑性和通过损伤和未损伤纤维的侧支发芽形成新回路是这种自发恢复过程的重要组成部分。我们的研究主要集中在中枢神经系统中受损神经网络的再生和可塑性。尽管过去认为成年人中枢神经系统损伤后不能再生，但这一发现揭示了成年人中枢神经系统损伤后神经回路可塑性的机制。

In the adult mammalian central nervous system(CNS), it is well known that injured axons exhibit very limited regeneration ability. Due to this lack of appropriate axonal regeneration, a traumatic damage to the adult brain and spinal cord frequently causes permanent neuronal deficits such as paralysis. Several axon growth inhibitors in the CNS have been identified in the myelin. These proteins contribute to the lack of regeneration of the injured CNS. However, it is noted that spontaneous functional recovery sometimes occurs following CNS injury. Synaptic plasticity in pre-existing pathways and the formation of new circuits through collateral sprouting of lesioned and unlesioned fibers are important components of this spontaneous recovery process. Our research has focused on regeneration and plasticity of destructed neural network in the CNS. It unveiled the mechanism of plasticity of neural circuit after injury to the adult CNS, although it had been believed that adult CNS does not regenerate if damaged.