Niclou Simone P, Ehlert Erich M E, Verhaagen Joost
Netherlands Institute for Brain Research, Laboratory for Neuroregeneration, Amsterdam, The Netherlands.
J Neurotrauma. 2006 Mar-Apr;23(3-4):409-21. doi: 10.1089/neu.2006.23.409.
Regenerating axons stop growing when they reach the border of the glial-fibrotic scar, presumably because they encounter a potent molecular barrier inhibiting growth cone advance. Chemorepulsive axon guidance molecules provide a non-permissive environment restricting and channeling axon growth in the developing nervous system. These molecules could also act as growth-inhibitory molecules in the regenerating nervous system. The receptors for repulsive guidance cues are expressed in the mature nervous system, suggesting that adult neurons are sensitive to the activity of developmentally active repulsive proteins. In this review, we summarize recent observations on semaphorins, ephrins, and slits in the injured brain and spinal cord, providing evidence that these proteins are major players in inhibiting axonal regeneration and establishing the glial-fibrotic scar.
再生轴突到达神经胶质纤维化瘢痕边界时会停止生长，推测是因为它们遇到了一种强大的分子屏障，抑制了生长锥的前进。化学排斥性轴突导向分子提供了一个不允许轴突生长的环境，在发育中的神经系统中限制并引导轴突生长。这些分子在再生神经系统中也可能作为生长抑制分子发挥作用。排斥性导向信号的受体在成熟神经系统中表达，这表明成年神经元对发育活跃的排斥性蛋白的活性敏感。在这篇综述中，我们总结了近期关于损伤脑和脊髓中信号素、 Ephrin 蛋白和缝隙连接蛋白的观察结果，提供了证据表明这些蛋白是抑制轴突再生和形成神经胶质纤维化瘢痕的主要因素。
