Ludwin S K
Department of Pathology, Kingston General Hospital, Ontario, Canada.
Acta Neuropathol. 1990;80(2):184-91. doi: 10.1007/BF00308922.
The long-term survival of oligodendrocytes in the absence of axons in adult animals was studied following Wallerian degeneration of the optic nerves of adult rats for periods up to 22 months. In contrast to the findings in development and in young animals, large numbers of oligodendrocytes survived during this time period even when deprived of axonal stimuli. The morphological phenotype of many of these cells differed from those of normal oligodendrocytes, and their oligodendrocytic nature was confirmed at a light microscopic level using antibodies to carbonic anhydrase, and at an electron microscopic level by using antibodies to myelin oligodendrocyte glycoprotein. Although there did appear to be some loss of oligodendrocytes over time, a large proportion appeared to remain intact. Many of the remaining cells and processes appeared to resemble resting or quiescent cells. The survival of these cells demonstrates the differential susceptibility of mature and developing oligodendrocytes to loss of axonal stimulus and also indicates a possible reserve capacity for repair following central nervous system injury.
在成年大鼠视神经发生华勒氏变性后长达22个月的时间里,研究了成年动物中少突胶质细胞在无轴突情况下的长期存活情况。与发育阶段和幼年动物中的发现相反,即使在缺乏轴突刺激的情况下,大量少突胶质细胞在这段时间内仍能存活。其中许多细胞的形态表型与正常少突胶质细胞不同,通过使用碳酸酐酶抗体在光学显微镜水平以及使用髓鞘少突胶质细胞糖蛋白抗体在电子显微镜水平证实了它们的少突胶质细胞性质。尽管随着时间的推移确实似乎有一些少突胶质细胞丢失,但很大一部分似乎保持完整。许多剩余的细胞和突起似乎类似于静息或静止细胞。这些细胞的存活证明了成熟和发育中的少突胶质细胞对轴突刺激丧失的敏感性差异,也表明中枢神经系统损伤后可能存在修复的储备能力。