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朗飞结以及结侧区是有鞘轴突上的一些极化区域,越来越多的证据表明胶质细胞分泌的某些抑制中枢神经系统损伤后轴突再生过程中神经突起生长的分子如粘蛋白(tenascins)、硫酸软骨素蛋白聚糖(chondroitin sulphate pro-teoglycans)、髓鞘相关糖蛋白(myelin-associated glycopro-tein,MAG)、轴突生长抑制因子(Nogo)以及少突胶质细胞髓鞘糖蛋白(OMGP)等非常特异性的富集于朗飞结区域。这些分子在体外组织培养过程中显示出强烈的神经突起生长抑制作用。在一些基因无义突变的动物模型,能够观察到朗飞结处轴突的生长,表明这些抑制分子能够生理性地保持轴突的完整性并且阻止轴突间随机和错误的联结,然而,大部分的基因无义突变动物模型显示不出明显的中枢神经系统再生改善。这些被称为抑制因子的分子是否是神经再生失败的真正元凶这些抑制因子体内体外实验结果的不一致以及它们特异的定位分布让我们有理由对它们在其他生理作用和功能方面进行重新评价。考虑到轴突-胶质细胞相互作用的双向特性,本综述认为这些抑制因子不仅通过神经元上的受体信号通路调节轴突的极化、离子通道的功能以及轴突的分枝,另一方面轴突产生的化学分子也能反馈性的通过朗飞结区域寡突胶质细胞上的胶质细胞受体信号通路影响寡突胶质细胞的发育。
Long-flying junction and junctional region are some of the polarized areas on the sheath axons. There is increasing evidence that some of the molecules secreted by glial cells that inhibit the growth of neurites during axonal regeneration following injury to the central nervous system such as Tenascins, chondroitin sulphate pro-teoglycans, myelin-associated glycopro-tein (MAG), axon growth inhibitory factor (Nogo) and oligodendrocytes Myelin glycoprotein (OMGP) and other very specific enrichment in the Langfang junction area. These molecules show strong inhibition of neurite outgrowth during in vitro tissue culture. In animal models of genetically nonsense mutations, the growth of axons at the Lanfar junction can be observed, suggesting that these inhibitory molecules are able to sustain axonal integrity physiologically and prevent random and erroneous association between axons, however, large Some animal models of nonsense mutations showed no significant CNS regeneration improvement. Whether these molecules, known as inhibitors, are the real culprits for the failure of nerve regeneration, and the inconsistent results of in vitro and in vivo experiments with these inhibitors and their specific localization allows us to justify their re-evaluation of other physiological roles and functions. Considering the bi-directional nature of axonal-glial interactions, the review suggests that these inhibitors not only regulate axonal polarization, ion channel function, and axonal branching not only through receptor signaling pathways on neurons, but also Aspects of the chemical molecules produced by axons can also affect the development of oligodendrocytes through the glial cell receptor signaling pathway on the oligodendrocyte in the Longfei junction region.