OLIGODENDROGLIA: MYELINATION AND DEMYELINATION

在中枢神经系统中，少突胶质细胞广泛分布 形成包裹节段的多层髓鞘 以增强神经冲动的跳跃性传导。除了……之外 负责这一膜的合成的还有少突胶质细胞 在动物的一生中保持它。在髓磷脂的高峰期 生产，据计算，该细胞类型可能合成更多 每天在髓鞘膜中的重量是自己的三倍。在疾病方面 以脱髓鞘为特征的少突胶质细胞可能是靶细胞，并且 它的表面成分可能特别重要。我们相信，到 少突胶质细胞血浆中蛋白质和糖蛋白的研究 膜及其在正常人和疾病患者中的基因调控 我们或许能够理解脱髓鞘的机制 在分子水平上的过程。我们已经确认并正在提纯两个 质膜中的主要糖蛋白，通常不存在于 髓鞘，但存在于患者受影响的髓鞘和膜中 患有异色性脑白质营养不良。单抗和兔抗血清 将针对这些纯化的糖蛋白生产，作为工具用于 确定糖蛋白是否是少突胶质细胞和 以提纯大量的糖蛋白进行化学分析。我们的龙 学期目标是研究这两种糖蛋白在脑内的调节。 正常状态和脱髓鞘过程中的少突胶质细胞。 在其他研究中，我们计划修改我们的差示电镀方法 从新生大鼠脑中获取少突胶质细胞并从小鼠体内获取 大脑。一旦获得小鼠少突胶质细胞，它们将被鉴定 通过免疫荧光、电子显微镜和掺入研究，以及 与大鼠和大鼠的少突胶质细胞进行比较 牛脑。然后，将从震颤和 Jimpy突变小鼠品系(髓鞘形成异常模型或 下髓鞘作用)直接比较表面抗原、形态和 正常细胞的功能。从这些突变体中纯化的少突胶质细胞 到目前为止，还没有对老鼠进行研究。我们的长期目标是研究基因 在发育和疾病中的分子水平上的表达。

In the central nervous system, oligodendroglia elaborate extensive amounts of membranes to form the multilamellar myelin sheath which enfolds segments of axons to enhance saltatory conduction of nerve impulses. In addition to being responsible for the synthesis of this membrane, oligodendroglia also maintain it during the lifetime of the animal. During the peak of myelin production, it has been calculated that this cell type may synthesize more than three times its own weight in myelin membranes each day. In diseases chracterized by demyelination, oligodendroglia may be the target cell, and its surface components may be of particular importance. We believe that by studying the proteins and glycoproteins in oligodendroglial plasma membranes, and their genetic regulation in both the normal and diseased state, we may be able to understand the mechanism of the demyelinating process at the molecular level. We have identified and are purifying two major glycoproteins in plasma membranes that are not normally present in myelin, but are present in affected myelin and membranes from a patient with metachromatic leucodystrophy. Both monoclonal and rabbit antiserum will be produced against these purified glycoproteins for use as tools to determine if the glycoproteins are surface markers for oligodendroglia and to purify larger amounts of glycoproteins for chemical analysis. Our long term goals are to study the regulation of these two glycoproteins in oligodendroglia in the normal state and during demyelination. In other studies we plan to modify our differential plating method for obtaining oligodendroglia from neonatal rat brain to obtain them from mouse brain. Once mouse oligodendroglia are obtained, they will be characterized by immunofluorescence, electron microscopy, and incorporation studies, and the results compared with those oligodendroglia obtained from rat and bovine brain. Then oligodendroglia will be prepared from the Quaking and the Jimpy mutant mouse strains (models of abnormal myelin formation or of hypomyelination) to directly compare surface antigens, morphology, and function with normal cells. Purified oligodendroglia from these mutant mice have not been studied thus far. Our long term goals are to study gene expression at the molecular level during development and in disease.