REGENERATION OF OLIGODENDROGLIA DURING RECOVERY FROM DEMYELINATING DISEASE
REGENERATION OF OLIGODENDROGLIA DURING RECOVERY FROM DEMYELINATING DISEASE
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DOI：
10.1126/science.190678
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发表时间：
1977-01-01
期刊：
影响因子：
56.9
通讯作者：
WEINER, LP
中科院分区：
文献类型：
--
作者：
HERNDON, RM;PRICE, DL;WEINER, LP
小鼠肝炎病毒 JHM 株感染后，由于少突神经胶质细胞的溶细胞性感染，导致脱髓鞘。在恢复过程中，动物表现出髓鞘再生，这可能是由于幸存的少突胶质细胞扩展其领土或由于产生新的少突胶质细胞所致。使用 3 H 标记的胸苷进行的 EM 放射自显影研究表明，与髓鞘再生相关的细胞是新生成的少突神经胶质细胞。
Infection of mice with the JHM strain of mouse hepatitis virus causes demyelination as a result of a cytolytic infection of oligodendroglia. In recovery, animals show remyelination, which could result either from surviving oligodendrocytes extending their territory or by generation of new oligodendroglia. EM autoradiographic studies with 3H-labeled thymidine demonstrate that the cells associated with remyelination are newly generated oligodendroglia.