再髓鞘化
少突胶质细胞
神经科学
生物
轴突
人口
髓鞘
前体细胞
细胞生物学
神经上皮细胞
神经胶质
胶质瘢痕
免疫学
中枢神经系统
细胞
星形胶质细胞
神经干细胞
干细胞
医学
环境卫生
遗传学
作者
Joel M. Levine,Richard Reynolds,James W. Fawcett
标识
DOI:10.1016/s0166-2236(00)01691-x
摘要
Adult oligodendrocyte precursor cells (OPCs) make up around 5-8% of the glial cell population in the CNS. Their function in the undamaged CNS is largely unknown, but their processes are in contact with nodes of Ranvier and synapses, suggesting a regulatory role at these structures. The cells divide slowly, and constitute approximately 70% of cells labelled following a pulse injection of bromodeoxyuridine. In the injured CNS the cells form a reactive glial population that undergoes hypertrophy and mitosis, probably driven by a variety of growth factors and cytokines. In response to demyelination they divide and are thought to differentiate to provide new oligodendrocytes to replace those that have been lost. However, remyelination fails during the later stages of multiple sclerosis, and it is not clear whether this is as a result of a depletion of adult OPCs, inhibition within the glial scar, or damage to the axons that prevents myelination. Adult OPCs are also activated and proliferate following other forms of CNS damage, such as mechanical injury, excitotoxicity and viral infection. The cells produce several of the chondroitin sulphate proteoglycans that might inhibit axon regeneration.
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