Papasozomenos S C, Autilio-Gambetti L, Gambetti P
J Cell Biol. 1981 Dec;91(3 Pt 1):866-71. doi: 10.1083/jcb.91.3.866.
beta, beta'-Iminodipropionitrile (IDPN), a synthetic compound that selectively impairs slow axonal transport, produced a rearrangement of the axonal cytoskeleton, smooth endoplasmic reticulum, and mitochondria. Immunoperoxidase staining using an antiserum to the 68,000-dalton neurofilament subunit demonstrated a displacement of neurofilaments toward the periphery of the axons of IDPN-treated rats. This change occurred simultaneously along the entire length of the sciatic nerve. Ultrastructural morphometry of the axonal organelles confirmed the peripheral relocation of neurofilaments and also showed a displacement of microtubules, smooth endoplasmic reticulum, and mitochondria to the center of the axons. The overall density of axonal mitochondria was increased, whereas those of other organelles were not significantly changed. Axons were reduced in size by 10--24%, the large axons being more affected than the small ones. The observed rearrangement of axonal organelles may be due to an effect of IDPN on microtubule-neurofilament interactions, which could in turn explain the impairment of the slow transport. Axons in IDPN intoxication are a useful model to study the organization of the axoplasm and the mechanism of axonal transport.
β,β'-亚氨基二丙腈(IDPN)是一种能选择性损害轴突慢速运输的合成化合物,它导致轴突细胞骨架、滑面内质网和线粒体发生重排。使用针对68,000道尔顿神经丝亚基的抗血清进行免疫过氧化物酶染色显示,在经IDPN处理的大鼠轴突中,神经丝向轴突外周移位。这种变化在坐骨神经的整个长度上同时发生。轴突细胞器的超微结构形态计量学证实了神经丝的外周重新定位,还显示微管、滑面内质网和线粒体向轴突中心移位。轴突线粒体的总体密度增加,而其他细胞器的密度没有显著变化。轴突大小缩小了10% - 24%,大轴突比小轴突受影响更大。观察到的轴突细胞器重排可能是由于IDPN对微管 - 神经丝相互作用的影响,这反过来可以解释慢速运输的损害。IDPN中毒的轴突是研究轴浆组织和轴突运输机制的有用模型。