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钙离子载体离子霉素在体内诱导的中枢脱髓鞘。

Central demyelination induced in vivo by the calcium ionophore ionomycin.

作者信息

Smith K J, Hall S M

机构信息

Division of Anatomy and Cell Biology, United Medical School, London, UK.

出版信息

Brain. 1994 Dec;117 ( Pt 6):1351-6. doi: 10.1093/brain/117.6.1351.

DOI:10.1093/brain/117.6.1351
PMID:7820571
Abstract

The effects of injecting the calcium-selective ionophore, ionomycin, into myelinated tracts in the dorsal columns of adult rat spinal cords were examined electron microscopically. In vivo, ionomycin induced a primary vesicular demyelination, together with a variable degree of axonal degeneration, in a dose-dependent manner. The results are consistent with previous demonstrations that mature oligodendrocytes are more vulnerable to alterations in levels of [Ca2+]i than other glial cells. We speculate that demyelination induced by ionomycin in vivo occurs as a result of direct activation of endogenous Ca(2+)-dependent enzymes and/or as a consequence of oligodendrocyte injury mediated via astrocytes.

摘要

通过电子显微镜检查了向成年大鼠脊髓背柱有髓神经纤维束中注射钙选择性离子载体离子霉素的效果。在体内,离子霉素以剂量依赖的方式诱导了原发性水泡性脱髓鞘,并伴有不同程度的轴突变性。这些结果与先前的证明一致,即成熟少突胶质细胞比其他神经胶质细胞更容易受到细胞内钙离子([Ca2+]i)水平变化的影响。我们推测,离子霉素在体内诱导的脱髓鞘是内源性钙依赖性酶直接激活的结果,和/或通过星形胶质细胞介导的少突胶质细胞损伤的结果。

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