Neurogenesis in the adult spinal cord in an experimental model of multiple sclerosis
Neurogenesis in the adult spinal cord in an experimental model of multiple sclerosis
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DOI：
10.1111/j.1460-9568.2005.04563.x
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发表时间：
2006-01-01
影响因子：
3.4
通讯作者：
Brundin, L
中科院分区：
文献类型：
--
作者：
Danilov, AI;Covacu, R;Brundin, L
多发性硬化是一种以炎症、脱髓鞘、轴突变性和神经功能障碍积累为特征的中枢神经系统炎症性疾病。在此之前，我们证明了干细胞可能是髓鞘再生的内源性来源。我们现在讨论的问题是，神经发生是否可以发生在神经炎性病变。我们证明，在实验性自身免疫性脑脊髓炎中，大鼠诱导的1,1'-二十八烷基-6,6'-二（4硫戊基）-3,3,3‘,3’四甲基多碳青蛋白（DiI）标记的室管膜细胞不仅增殖，而且后代迁移到神经炎症区域并分化为表达神经元标记物β - iii -微管蛋白和NeuN的细胞。此外，这些细胞对溴脱氧尿苷和PCNA（细胞增殖的标志物）具有免疫反应。我们利用全细胞膜片钳技术对从脊髓病变中新分离的dii标记细胞进行了研究，证明了这些细胞具有类似于未成熟神经元的超调动作电位的能力。因此，我们为成人脊髓神经炎性病变中神经发生的起始提供了第一个证据。
Multiple sclerosis is an inflammatory disease of the central nervous system characterized by inflammation, demyelination, axonal degeneration and accumulation of neurological disability. Previously, we demonstrated that stem cells constitute a possible endogenous source for remyelination. We now addressed the question of whether neurogenesis can occur in neuroinflammatory lesions. We demonstrated that, in experimental autoimmune encephalomyelitis, induced in rats 1,1'-dioctadecyl-6,6'-di(4sulphopentyl)-3,3,3',3'tetramethylindocarbocyanin(DiI)-labelled ependymal cells not only proliferated but descendants migrated to the area of neuroinflammation and differentiated into cells expressing the neuronal markers beta-III-tubulin and NeuN. Furthermore, these cells were immunoreactive for bromodeoxyuridine and PCNA, markers for cells undergoing cell proliferation. Using the whole-cell patch-clamp technique on freshly isolated 1, DiI-labelled cells from spinal cord lesions we demonstrated the ability of these cells to fire overshooting action potentials similar to those of immature neurones. We thus provide the first evidence for the initiation of neurogenesis in neuroinflammatory lesions in the adult spinal cord.