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溴化乙锭诱导猫脊髓脱髓鞘。

Ethidium bromide induced demyelination in the spinal cord of the cat.

作者信息

Blakemore W F

出版信息

Neuropathol Appl Neurobiol. 1982 Sep-Oct;8(5):365-75. doi: 10.1111/j.1365-2990.1982.tb00305.x.

Abstract

Small volumes of ethidium bromide were injected into the dorsal column of the spinal cord of cats. Oligodendrocytes and astrocytes showed morphological evidence of intoxication by ethidium bromide from 2 days after injection. However, apart from around the point of injection and the needle tract, demyelination did not occur until between 8 and 14 days. Both oligodendrocytes and astrocytes were absent from the demyelinated area at 14 days and all but a small number of demyelinated axons were remyelinated by Schwann cells. These cells first appeared in the lesion at 10 days, but axon association and myelination did not occur until 16 days. This model of experimental demyelination indicates once again that Schwann cell invasion of demyelinated areas in the CNS occurs if both oligodendrocytes and astrocytes are destroyed. None of the lesions in the present investigation were in continuity with root entry zones, indicating that this location is not a prerequisite for Schwann cell invasion of the CNS.

摘要

将少量溴化乙锭注入猫脊髓的背柱。从注射后2天起,少突胶质细胞和星形胶质细胞就显示出溴化乙锭中毒的形态学证据。然而,除了注射点和针道周围外,直到8至14天之间才发生脱髓鞘。在14天时,脱髓鞘区域没有少突胶质细胞和星形胶质细胞,除了少数脱髓鞘轴突外,所有轴突都被施万细胞重新髓鞘化。这些细胞在10天时首次出现在病变处,但直到16天时轴突才与施万细胞结合并开始髓鞘化。这种实验性脱髓鞘模型再次表明,如果少突胶质细胞和星形胶质细胞都被破坏,中枢神经系统脱髓鞘区域会发生施万细胞侵入。本研究中的病变均与神经根进入区不连续,表明该位置不是施万细胞侵入中枢神经系统的先决条件。

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