神经胶质生物学和疾病。

N Baumann, A Baron-Van Evercooren, C Jacque, B Zalc
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引用次数: 0

摘要

在生长因子和细胞因子的定位和表达模式方面,今年已经投入了大量的工作。虽然不可能直接从体外推断出体内的情况,但胶质细胞的可塑性似乎受生长因子的影响很大。在正常情况下,体内星形胶质细胞不表达许多生长因子,但病理事件可以解除这些限制。细胞因子及其受体已定位于神经元或胶质细胞类型。在神经元中发现的程序性细胞死亡似乎也发生在少突胶质细胞中,并可能受到存活因素的影响。在成人大脑中,胶质祖细胞是存在的,可能是产生髓鞘少突胶质细胞用于髓鞘修复的潜在来源。在周围神经系统中,轴突-雪旺细胞信号在发育过程中可能在两个方向上起作用。一些动物神经系统突变体是人类疾病的模型;其中之一,颤栗鼠,已经有效地导致了1a型沙克-玛丽-图斯病的遗传特征。至于髓鞘破坏,脱髓鞘与炎症的关系还不是很清楚。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glial biology and disorders.

Much work has been devoted this year to the localization and mode of expression of growth factors and cytokines. Although it is not possible to extrapolate directly from in vitro to in vivo conditions, the plasticity of glial cells seems to be very influenced by growth factors. Astrocytes in vivo do not express many growth factors during normal conditions, but a pathologic event can lift these restrictions. Cytokines and their receptors have been localized on neuronal or glial cell types. The programmed cell death, well identified in neurons, seems to occur also in oligodendrocytes and may be influenced by survival factors. In the adult brain, glial progenitors are present and may be a potential source to generate myelinating oligodendrocytes for myelin repair. In the peripheral nervous system, axonal-Schwann cell signaling may function in both directions during development. Some animal neurologic mutants are models for human diseases; one of them, the Trembler mouse, has effectively led to the genetic characterization of Charcot-Marie-Tooth disease type 1a. As for myelin destruction, the relationship between demyelination and inflammation is still not very clear.

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