Song Xing-Yun, Zhong Jin-hua, Wang Xin, Zhou Xin-Fu
Department of Human Physiology and Centre for Neuroscience, Flinders University, Adelaide 5001, Australia.
J Neurosci. 2004 Jan 14;24(2):542-6. doi: 10.1523/JNEUROSCI.4281-03.2004.
The neurotrophin receptor p75NTR is the coreceptor for Nogo receptor, mediating growth cone collapse in vitro by MAG, myelin oligodendrocyte glycoprotein (Omgp), and Nogo. Whether p75NTR plays any role in the failure of nerve regeneration in vivo is not known. Immunohistochemical data showed that p75NTR was expressed in only a very small subset of ascending sensory axons but not in any corticospinal axons in the dorsal column of either normal or injured spinal cord. Using p75NTR-deficient mice, we showed that the depletion of the functional p75NTR did not promote the regeneration of the descending corticospinal tract and ascending sensory neurons in the spinal cord 2 weeks after spinal cord injury. Local administration of p75NTR-Fc fusion molecule, the dominant-negative receptor to block the function of neurite outgrowth inhibitors, did not improve regeneration of ascending sensory neurons in the injured spinal cord. Our results suggest that p75NTR may not be a critical molecule mediating the function of myelin-associated inhibitory factors in vivo.
神经营养因子受体p75NTR是Nogo受体的共受体，在体外介导髓鞘相关糖蛋白（MAG）、髓鞘少突胶质细胞糖蛋白（Omgp）和Nogo引起的生长锥塌陷。p75NTR在体内神经再生失败中是否起作用尚不清楚。免疫组织化学数据显示，在正常或损伤脊髓的背柱中，p75NTR仅在极少数上升感觉轴突中表达，而在任何皮质脊髓轴突中均不表达。利用p75NTR基因敲除小鼠，我们发现功能性p75NTR的缺失在脊髓损伤后2周并未促进脊髓中下行皮质脊髓束和上升感觉神经元的再生。局部给予p75NTR-Fc融合分子（一种阻断神经突生长抑制因子功能的显性负性受体）并不能改善损伤脊髓中上升感觉神经元的再生。我们的结果表明，p75NTR可能不是体内介导髓鞘相关抑制因子功能的关键分子。
