CELLULAR EVENTS IN MYELINATION

髓鞘，在中枢神经系统中由 少突胶质细胞与神经元的突起密切相关。 起到促进神经冲动传导的作用。形成了一种 髓鞘是神经系统发育的重要部分， 髓鞘在人类神经病理条件下的破坏，如 多发性硬化症与功能急剧恶化有关。 这里提出的研究旨在了解细胞 在发育过程中促进髓鞘形成的机制， 以及脱髓鞘疾病修复过程中对其的改造。这个 增殖的前体细胞形成少突胶质细胞 必然是中枢神经系统髓鞘形成的第一步 系统；然而，对前体细胞知之甚少。这些研究 将通过组合来探测前体细胞的生化同一性 胸腺嘧啶核苷放射自显影和免疫细胞化学染色 增殖中的少突胶质前体细胞是否含有 髓鞘特异性蛋白、髓鞘碱性蛋白和髓鞘相关蛋白 糖蛋白，如果没有，在细胞停止后的什么时间 分裂这些蛋白质出现在发育中的少突胶质细胞中。 此外，髓鞘碱性蛋白免疫反应性的变化和 髓鞘相关糖蛋白将与细胞细小变化相关 结构。神经胶质细胞的产生也将分两个阶段进行研究。 小鼠的遗传性疾病，颤抖和颤抖，产生过剩 少突胶质细胞的数量。对这种生产过剩的研究可能会给出线索 刺激正常人少突胶质细胞形成的机制 发育和重新髓鞘形成。建议的分析将确立 一种发育时期，在此期间过剩的细胞在 突变体，使用定量光显微镜和电子显微镜。中的胶体生成 然后用胸腺嘧啶核苷放射自显影检查突变株 免疫细胞化学，以发现是否过量生产 少突胶质细胞与具有相似特征的干细胞相关 符合或不同于为正常发展而建立的。

Myelin sheaths, elaborated in the central nervous system by oligodendrocytes, are intimately associated with the processes of neurons and act to facilitate the conduction of nerve impulses. The formation of myelin is a prominent part of the development of the nervous system, and the disruption of myelin in human neuropathological conditions such as multiple sclerosis is associated with dramatic deterioration of function. The studies proposed here are aimed at understanding the cellular mechanisms which contribute to the formation of myelin during development, and to its reformation during repair from demyelinating disease. The formation of oligodendrocytes from proliferating precursor cells is necessarily the first step in myelin formation in the central nervous system; however, the precursor cell is poorly understood. These studies will probe the biochemical indentity of the precursor cell by a combination of thymidine autoradiography and immunocytochemical staining, to determine whether the proliferating oligodendrocyte precursor cells contain the myelin specific protiens, myelin basic protein and myelin-associated glycoprotein and, if they do not, at what time after cessation of cell division these proteins appear in the developing oligodendrocytes. Furthermore, changes in immunoreactivity for myelin basic protein and myelin-associated glycoprotein will be correlated with changes in cell fine structure. The production of neuroglial cells will also be studied in two genetic disorders of mouse, quaking and shiverer, which produce excess numbers of oligodendrocytes. Study of this overproduction may give clues to the mechanisms which stimulate oligodendrocyte formation in normal development and in remyelination. The analysis proposed will establish the period of development during which the excess cells are formed in the mutants, using quantitative light and electron microscopy. Gliogenesis in the mutants wil then be examined by thymidine autoradiography and immunocytochemistry, to discover whether the overproduction of oligodendrocytes is associated with stem cells with characteristics similar to or different from those established for normal development.