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小鼠中的病毒诱导性脱髓鞘:少突胶质细胞的“逆行性死亡”

Virus-induced demyelination in mice: "dying back" of oligodendrocytes.

作者信息

Rodriguez M

出版信息

Mayo Clin Proc. 1985 Jul;60(7):433-8. doi: 10.1016/s0025-6196(12)60865-9.

Abstract

Demyelination was produced in mice by intracerebral inoculation of Theiler's murine encephalomyelitis virus. The earliest ultrastructural changes occurred in the inner cytoplasmic tongues of oligodendrocytes, the most distal extension of these cells. Viral antigen was localized to glial loops that connect with myelin lamellae. This study indicates that a "dying-back" process may occur in virus-infected oligodendrocytes, which then results in demyelination.

摘要

通过脑内接种泰勒氏鼠脑脊髓炎病毒在小鼠中产生脱髓鞘。最早的超微结构变化发生在少突胶质细胞的胞质内舌状突起,即这些细胞最远端的延伸部分。病毒抗原定位于与髓鞘板层相连的神经胶质环。这项研究表明,在病毒感染的少突胶质细胞中可能发生“逆行性变性”过程,进而导致脱髓鞘。

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