Mason J L, Jones J J, Taniike M, Morell P, Suzuki K, Matsushima G K
UNC Neuroscience Center and Curriculum in Neurobiology, University of North Carolina, Chapel Hill, North Carolina 27599, USA.
J Neurosci Res. 2000 Aug 1;61(3):251-62. doi: 10.1002/1097-4547(20000801)61:3<251::AID-JNR3>3.0.CO;2-W.
We have documented changes in the oligodendrocyte population during demyelinating insult to the adult CNS. Feeding of cuprizone to adult mice led to apoptotic death of mature oligodendrocytes followed by profound demyelination of the corpus callosum. A regenerative response was initiated even during active demyelination. Oligodendrocyte progenitors have begun to proliferate and then accumulate within the lesion. Many of these cells may have migrated from the sub-ventricular zone and fornix before their accumulation in the demyelinating corpus callosum. The accumulation of differentiating oligodendrocyte progenitors was followed closely by the reappearance of mature oligodendrocytes and remyelination. Interestingly, an increase in IGF-1 mRNA was detected at Week 3 through Week 7, suggesting potential involvement in remyelination. Other factors, however, such as PDGF, NT3, FGF, jagged, and notch remained unchanged. These results suggest that the mature oligodendroglial population depleted by apoptosis is replaced by a newly formed oligodendroglial population derived from progenitors; these accumulate and seem to differentiate during remyelination.
我们已经记录了成年中枢神经系统脱髓鞘损伤过程中少突胶质细胞群体的变化。给成年小鼠喂食铜螯合剂导致成熟少突胶质细胞凋亡死亡,随后胼胝体出现严重脱髓鞘。即使在活跃的脱髓鞘过程中也启动了再生反应。少突胶质前体细胞开始增殖,然后在损伤部位聚集。这些细胞中的许多可能在聚集到脱髓鞘的胼胝体之前,从脑室下区和穹窿迁移而来。分化中的少突胶质前体细胞聚集之后,紧接着成熟少突胶质细胞重新出现并发生髓鞘再生。有趣的是,在第3周通过第7周检测到IGF-1 mRNA增加,提示其可能参与髓鞘再生。然而,其他因子,如血小板衍生生长因子(PDGF)、神经营养因子3(NT3)、成纤维细胞生长因子(FGF)、锯齿蛋白和Notch蛋白则保持不变。这些结果表明,因凋亡而减少的成熟少突胶质细胞群体被源自前体细胞的新形成的少突胶质细胞群体所取代;这些细胞在髓鞘再生过程中聚集并似乎发生分化。