Direct observation of myelination in vivo in the mature human central nervous system - A model for the behaviour of oligodendrocyte progenitors and their progeny
Direct observation of myelination in vivo in the mature human central nervous system - A model for the behaviour of oligodendrocyte progenitors and their progeny
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DOI：
10.1093/brain/120.11.2071
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发表时间：
1997-11-01
期刊：
影响因子：
14.5
通讯作者：
Rodriguez, M
中科院分区：
文献类型：
--
作者：
Hunter, SF;Leavitt, JA;Rodriguez, M
我们研究了人视网膜中CNS髓鞘的斑块，以确定髓鞘形成的模式和轴突的局部影响。我们分析了47只眼（37名成人和2名青少年）60个视网膜髓鞘斑块中神经纤维层的位置、面积和厚度。对4只眼睛的5个贴片进行了6-11年的连续研究。神经纤维层的厚度是从灵长类动物视网膜的图谱中获得的，然后估计每个补丁的有髓组织的体积。视网膜髓鞘形成有三种模式：与视盘相邻的厚斑块（I型）;与视盘分离的薄条纹状斑块（II型）;或与严重弱视相关的后极大量髓鞘形成（III型）。乳头状斑束也没有髓鞘在I型和II型和相对幸免于III型补丁，这表明迁移少突胶质细胞祖细胞不支持这些轴突。局部神经纤维层决定了焦斑的大小，定量髓鞘形成明显，斑块体积的峰值在0.16和0.64 mm（3）。随着时间的推移，观察到在补丁边缘的髓鞘形成进展，与新的少突胶质细胞在成年期产生的假设一致。我们提出了一个理论模型，其中视网膜髓鞘形成的补丁是几个少突胶质细胞祖细胞表现出两种不同的行为的克隆后代。首先，高度迁移的无髓鞘的祖先使用较大的遗传学上较老的轴突作为运动的基质。其次，一个更成熟的祖细胞产生髓鞘少突胶质细胞以及进入成年生活，但只穿越很短的距离。利用这些数据，我们可以估计这些克隆中少突胶质细胞的数量和群体倍增时间。这项研究支持了轴突源性信号在调节人少突胶质细胞祖细胞行为和髓鞘形成中的作用。
We studied patches of CNS myelin in human retina in vivo to determine the pattern of myelination and the local influence of axons. We analysed the position, area and thickness of the nerve-fibre layer in 60 patches of retinal myelin in 47 eyes (in 37 adults and two adolescents). Five patches in four eyes were studied serially over 6-11 years. Nerve-fibre layer thickness was obtained from an atlas of primate retina, and volumes of myelinated tissue were then estimated for each patch. Retinal myelination occurred in three patterns: thick patches contiguous with the optic disc (type I); thin, striated patches detached from the disc (type II); or massive myelination of the posterior pole associated with severe amblyopia (type III). The papillomacular bundle did nor myelinate in types I and II and was relatively spared in type III patches, suggesting that migratory oligodendrocyte progenitors are not supported by these axons. The local nerve-fibre layer determined parch size, and quantal myelination was evident with modal peaks of patch volume at 0.16 and 0.64 mm(3). Myelination advanced at patch edges when observed over time, consistent with the hypothesis that new oligodendrocytes are produced in adulthood. We propose a theoretical model where patches of retinal myelination are the clonal progeny of a few oligodendrocyte progenitors exhibiting two different behaviours. First, a highly migratory, nonmyelinating progenitor uses larger phylogenetically older axons as the substrate for movement. Secondly, a more mature progenitor generates myelinating oligodendrocytes well into adult life, but traverses only short distances. Using this data, we can estimate the number of oligodendrocytes in these clones and population doubling-time. This study supports a role for axon-derived signals in the regulation of human oligodendrocyte progenitor behaviour and myelination in vivo.