Kalil K, Schneider G E
Brain Res. 1975 May 16;89(1):15-27. doi: 10.1016/0006-8993(75)90130-4.
Following lesions of the pyramidal tract in hamsters, retrograde changes were studied in the sensorimotor cortex and in the pyramidal tract axons proximal to the lesion, at survival times ranging from 2 weeks to 14 months. Severe cell shrinkage occurred in layer 5 pyramidal neurons as early as 2 weeks, but there was no cell loss among these neurons even with long survival times. Use of the Fink-Heimer method for degenerating axons revealed that the pyramidal tract proximal to the lesion had undergone a retrograde axon degeneration which, in some respects, resembled anterograde degeneration. The retrograde axon degeneration began at the lesion site and advanced slowly rostralwards with time involving increasingly greater numbers of fibers. However, even at the longest survival times the degeneration fell off markedly at pontine levels. The results indicate that this process represents a true retrograde fiber degeneration (as opposed to an indirect Wallerian degeneration) which appears to reach a point of equilibrium such that a partially shrunken pyramidal cell is maintaining a partially degenerated axon.
在仓鼠锥体束受损后，研究了感觉运动皮层以及损伤部位近端的锥体束轴突在2周到14个月的存活期内的逆行性变化。早在2周时，第5层锥体神经元就出现了严重的细胞萎缩，但即使存活时间很长，这些神经元中也没有细胞丢失。使用Fink-Heimer法检测变性轴突发现，损伤部位近端的锥体束发生了逆行性轴突变性，在某些方面类似于顺行性变性。逆行性轴突变性始于损伤部位，并随着时间缓慢向头端发展，涉及的纤维数量越来越多。然而，即使在最长的存活时间，脑桥水平的变性也明显减少。结果表明，这一过程代表了真正的逆行性纤维变性（与间接的华勒氏变性相反），似乎达到了一种平衡状态，即部分萎缩的锥体细胞维持着部分变性的轴突。
