Griffin J W, Hoffman P N, Clark A W, Carroll P T, Price D L
Science. 1978 Nov 10;202(4368):633-5. doi: 10.1126/science.81524.
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.
β,β'-亚氨基二丙腈(IDPN)的施用可阻止[35S]甲硫氨酸或[3H]亮氨酸标记的蛋白质在大鼠坐骨神经运动轴突中的正常慢速轴突运输。超微结构和电泳研究表明,神经丝三联体蛋白尤其保留在轴突起始的5毫米范围内,导致充满神经丝的轴突肿胀。快速顺行和逆行轴突运输不受影响。因此,IDPN选择性地损害了慢速轴突运输。该模型中的神经原纤维病理是神经丝慢速运输缺陷的结果。