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猫坐骨神经外植体培养中沃勒变性的观察

Observations on Wallerian degeneration in explant cultures of cat sciatic nerve.

作者信息

Crang A J, Blakemore W F

出版信息

J Neurocytol. 1986 Aug;15(4):471-82. doi: 10.1007/BF01611730.

Abstract

Wallerian degeneration was studied in vitro using explant cultures of cat sciatic nerve. As these cultures contain no macrophages they highlight the responses of Schwann cells to myelin sheath breakdown. Although there were regional variations in the changes observed in these cultures with respect to time, the sequence of events which lead to Schwann cell proliferation and to fragmentation and liberation of myelin debris into the endoneurial space was established. The initial event was rejection of myelin sheaths by Schwann cells. Liberated Schwann cells then proliferated within the basal lamina tube. In nerve fibres containing proliferating Schwann cells, myelin debris passed through breaks in the basal lamina tube into the endoneurial space. Schwann cells also escaped from the basal lamina tube with the myelin debris. Following the loss of the luminal contents the basal lamina tube collapsed and the intratubular Schwann cells formed bands of Büngner. The Schwann cells which migrated into the endoneurial space and subsequently onto the culture dish retained contact with each other. These studies indicate that rejection of myelin internodes by their supporting Schwann cells set in train a series of events in which Schwann cells and degenerating myelin behaved as separate components. Schwann cells were not involved in phagocytosis or degeneration of myelin. We conclude that Schwann cell proliferation in Wallerian degeneration is directed towards re-establishing cellular continuity within the basal lamina tube which is lost when Schwann cells reject their myelin sheaths.

摘要

利用猫坐骨神经外植体培养物在体外研究了华勒氏变性。由于这些培养物中不含巨噬细胞,它们突出了施万细胞对髓鞘崩解的反应。尽管在这些培养物中观察到的变化随时间存在区域差异,但导致施万细胞增殖以及髓鞘碎片断裂并释放到神经内膜间隙的事件顺序已确定。最初的事件是施万细胞排斥髓鞘。释放出来的施万细胞随后在基膜管内增殖。在含有增殖施万细胞的神经纤维中,髓鞘碎片通过基膜管的破裂处进入神经内膜间隙。施万细胞也与髓鞘碎片一起从基膜管中逸出。随着管腔内物质的流失,基膜管塌陷,管内的施万细胞形成了许旺氏带。迁移到神经内膜间隙并随后迁移到培养皿上的施万细胞彼此保持接触。这些研究表明,施万细胞对其支持的髓鞘节段的排斥引发了一系列事件,其中施万细胞和变性髓鞘表现为独立的成分。施万细胞不参与髓鞘的吞噬或变性。我们得出结论,华勒氏变性中施万细胞的增殖旨在重新建立基膜管内的细胞连续性,这种连续性在施万细胞排斥其髓鞘时会丧失。

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