Fawcett James W, Schwab Martin E, Montani Laura, Brazda Nicole, Müller Hans Werner
Cambridge University Centre for Brain Repair, Cambridge, UK.
Handb Clin Neurol. 2012;109:503-22. doi: 10.1016/B978-0-444-52137-8.00031-0.
Axon regeneration and the sprouting processes that underlie plasticity are blocked by inhibitory factors in the central nervous system (CNS) environment, several of which are upregulated after injury. The major inhibitory molecules are those associated with myelin and those associated with the glial scar. In myelin, NogoA, MAG, and OMgp are present on normal oligodendrocytes and on myelin debris. They act partly via the Nogo receptor, partly via an unidentified amino-Nogo receptor. In the glial scar, chondroitin sulphate proteoglycans, semaphorins, and the formation of a collagen-based membrane are all inhibitory. Methods to counteract these forms of inhibition have been identified, and these treatments promote axon regeneration in the damaged spinal cord, and in some cases recovery of function through enhanced plasticity.
轴突再生以及构成可塑性基础的发芽过程会被中枢神经系统（CNS）环境中的抑制因子所阻断，其中有几种抑制因子在损伤后会上调。主要的抑制分子是那些与髓磷脂相关的分子以及与胶质瘢痕相关的分子。在髓磷脂中，NogoA、MAG和OMgp存在于正常的少突胶质细胞和髓磷脂碎片上。它们部分通过Nogo受体起作用，部分通过一种未明确的氨基-Nogo受体起作用。在胶质瘢痕中，硫酸软骨素蛋白聚糖、信号素以及基于胶原蛋白的膜的形成都具有抑制作用。已经确定了对抗这些抑制形式的方法，这些治疗方法可促进受损脊髓中的轴突再生，并且在某些情况下通过增强可塑性来恢复功能。
