Slow axonal transport of neurofilament proteins: impairment of beta,beta'-iminodipropionitrile administration.
Slow axonal transport of neurofilament proteins: impairment of beta,beta'-iminodipropionitrile administration.
复制标题
神经丝蛋白的轴突运输缓慢：β,β-亚氨基二丙腈给药受损。
作者：
John W. Griffin;Paul N. Hoffman;Arthur W. Clark;Patrick T. Carroll;Donald L. Price
β，β ′-亚氨基二丙腈（IDPN）给药可阻止大鼠坐骨神经运动轴突中[35 S]甲硫氨酸或[3 H]亮氨酸标记蛋白的正常缓慢轴突转运。超微结构和电泳研究表明，神经丝三联体蛋白，特别是保留在最初的5毫米的轴突，导致神经胶质填充轴突selling。快速顺行和逆行轴突运输不受影响。IDPN因此选择性地损害慢轴突运输。该模型中的神经病理学是神经丝的缺陷性缓慢运输的结果。
beta,beta'-Iminodipropionitrile (IDPN) administration prevented normal slow axonal transport of [35S]methionine- or [3H]leucine-labeled proteins in rat sciatic motor axons. Ultrastructural and electrophoretic studies showed that the neurofilament triplet proteins in particular were retained within the initial 5 millimeters of the axons, resulting in neurofilament-filled axonal swellings. Fast anterograde and retrograde axonal transport were not affected. The IDPN thus selectively impaired slow axonal transport. The neurofibrillary pathology in this model is the result of the defective slow transport of neurofilaments.