Blakemore W F, Patterson R C
Acta Neuropathol. 1978 May 24;42(2):105-13. doi: 10.1007/BF00690975.
Rat and cat spinal cords were exposed to 2000, 3000 or 4000 rads of x-irradiation prior to producing an area of primary demyelination in the dorsal columns by the injection of lysolecithin. In animals irradiated with 4000 rads no remyelination by either Schwann cells or oligodendrocytes occurred. With 2000 rads both types of remyelination occurred, but when compared to unirradiated controls, central remyelination was less extensive, while Schwann cells remyelinated a greater percentage of axons. With 3000 rads the results were variable, some animals responded similarly to those in the 4000 rad group, whereas others responded as the 2000 rad animals. Oligodendrocytes were found among the persistently demyelinated axons in the 4000 rad animals and their processes were associated with, but only rarely formed a myelin sheath round, the demyelinated axons. It was concluded that irradiation damage to local cells was responsible for the inhibition of remyelination but it could not be determined if this was due to its effect on the oligodendrocytes alone. The origin of the oligodendrocytes found among the demyelinated axons is discussed in this context.
在通过注射溶血卵磷脂在背柱产生原发性脱髓鞘区域之前,将大鼠和猫的脊髓暴露于2000、3000或4000拉德的X射线照射下。在接受4000拉德照射的动物中,雪旺细胞或少突胶质细胞均未发生再髓鞘化。接受2000拉德照射时,两种类型的再髓鞘化均发生,但与未照射的对照组相比,中枢再髓鞘化范围较小,而雪旺细胞对更大比例的轴突进行了再髓鞘化。接受3000拉德照射时,结果各不相同,一些动物的反应与4000拉德组的动物相似,而另一些动物的反应则与2000拉德照射的动物相同。在接受4000拉德照射的动物中,在持续脱髓鞘的轴突中发现了少突胶质细胞,它们的突起与脱髓鞘轴突相关,但很少围绕脱髓鞘轴突形成髓鞘。得出的结论是,对局部细胞的辐射损伤是再髓鞘化受到抑制的原因,但无法确定这是否仅归因于其对少突胶质细胞的影响。在此背景下讨论了在脱髓鞘轴突中发现的少突胶质细胞的起源。