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轴突如何控制髓鞘形成?6-氨基烟酰胺神经病模型。

How do axons control myelin formation? The model of 6-aminonicotinamide neuropathy.

作者信息

Friede R L, Bischhausen R

出版信息

J Neurol Sci. 1978 Feb;35(2-3):341-53. doi: 10.1016/0022-510x(78)90014-x.

Abstract

Injection of 6-aminonicotinamide into young rats produces a peculiar neuropathy characterized by selective swelling and disruption of the layer of Schwann cell cytoplasm lining the inner surface of the myelin sheath. This layer increases greatly in volume, compressing the axon and distending the myelin sheath. Morphometry of such swollen fibers discloses that the amount of myelin in the distended sheaths is considerably greater than would correspond to the size of the axons, even if axonal compression is accounted for. The data favor the concept that sheath growth is stimulated by non-specific distension of the myelin sheath from inside.

摘要

向幼鼠注射6-氨基烟酰胺会产生一种特殊的神经病变,其特征是髓鞘内表面衬里的施万细胞细胞质层出现选择性肿胀和破坏。该层体积大幅增加,挤压轴突并使髓鞘膨胀。对这种肿胀纤维的形态测量表明,即使考虑到轴突受压,膨胀髓鞘中的髓磷脂量也远大于与轴突大小相对应的量。这些数据支持这样一种观点,即髓鞘的生长是由髓鞘从内部的非特异性扩张所刺激的。

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