缺血性损伤后小鼠脊髓轴突自发再生的研究

M. Euler, A. Janson, Jytte Overgaard Larsen, Åke Seiger, L. Forno, M. Bunge, Erik Sundström
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引用次数: 37

摘要

在这里,我们提供了证据,在成年大鼠脊髓损伤后,中枢神经系统轴突自发和持久的再生。在光化学诱导的缺血性脊髓损伤后,使用立体学工具估计200 kD神经丝(NF)免疫标记轴突的长度。与术后1周相比,病变腔内所有nf免疫标记轴突的总长度在病变后5、10和15周增加了6至10倍。在超微结构研究中,我们发现病灶内推定再生的轴突与少突胶质细胞或雪旺细胞有关,而其他纤维则无髓鞘。免疫组织化学表明,一些再生纤维具有酪氨酸羟化酶或血清素免疫反应性,表明其中心起源。这些发现表明,啮齿类动物脊髓损伤后存在相当数量的自发再生,并且这些纤维在损伤后仍存在数月。轴突中酪氨酸羟化酶和血清素免疫反应性的发现表明,下降的中央纤维有助于缺血性脊髓损伤的内源性修复。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Spontaneous Axonal Regeneration in Rodent Spinal Cord After Ischemic Injury
Here we present evidence for spontaneous and long-lasting regeneration of CNS axons after spinal cord lesions in adult rats. The length of 200 kD neurofilament (NF)-immunolabeled axons was estimated after photochemically induced ischemic spinal cord lesions using a stereological tool. The total length of all NF-immunolabeled axons within the lesion cavities was increased 6- to 10-fold at 5, 10, and 15 wk post-lesion compared with 1 wk post-surgery. In ultrastructural studies we found the putatively regenerating axons within the lesion to be associated either with oligodendrocytes or Schwann cells, while other fibers were unmyelinated. Immunohistochemistry demonstrated that some of the regenerated fibers were tyrosine hydroxylase- or serotonin-immunoreactive, indicating a central origin. These findings suggest that there is a considerable amount of spontaneous regeneration after spinal cord lesions in rodents and that the fibers remain several months after injury. The findings of tyrosine hydroxylase- and serotonin-immunoreactivity in the axons suggest that descending central fibers contribute to this endogenous repair of ischemic spinal cord injury.
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