Corrêa Clynton Lourenço, Allodi Silvana, Martinez Ana Maria Blanco
Departamento de Histologia e Embriologia, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Brain Behav Evol. 2005;66(3):145-57. doi: 10.1159/000087155. Epub 2005 Jul 25.
Wallerian degeneration is a very well described phenomenon in the vertebrate nervous system. In arthropods, and especially in crustaceans, nerve fiber degeneration has not been described extensively. In addition, literature shows that the events do not follow the same patterns as in vertebrates. In this study we report, by qualitative and quantitative ultrastructural analyses, the features and time course of the protocerebral tract degeneration following extirpation of the optic stalk. No remarkable changes were observed seven days after lesion. After 28 days the protocerebral tracts presented apparently preserved small and large diameter axons and some degenerating medium axons, with irregular contours and empty-looking aspect of the axoplasm. Forty days after the ablation of the optic stalks, both small (type I) and medium (type II and III) axons revealed signs of partial or total degeneration, but large nerve fibers (type IV) were still intact. After 45 days, the tract showed signs of advanced stage of degeneration and, apart from large axons, normal-looking fibers were almost absent. At these 3 last time points, degenerating axons displayed different electron densities and aspects, probably correlating to different onset times of the process. In addition, cells with granules in their cytoplasm, possibly hemocytes, were quite distinct, especially at 40 and 45 days after axotomy. These cells might share with glial cells the function of phagocytosis of cellular debris during the protocerebral tract degeneration. Quantitative analysis showed that the number of degenerating fibers increased significantly from 28 to 40 days after lesion, whereas the number of normal fibers decreased accordingly. Measurements of cross-sectional areas of normal and degenerating axons showed that types II and III (medium) start to degenerate before type I (small). Type IV (large) axons do not degenerate, even after 40 days. Therefore, we can conclude that degeneration in these afferent fibers starts late after axotomy, but proceeds at a faster rate afterwards until the complete degeneration of small and medium axons.
华勒氏变性是脊椎动物神经系统中一种已被充分描述的现象。在节肢动物中，尤其是甲壳类动物，神经纤维变性尚未得到广泛描述。此外，文献表明这些事件并不遵循与脊椎动物相同的模式。在本研究中，我们通过定性和定量超微结构分析，报告了视神经柄切除后脑前叶束变性的特征和时间进程。损伤后7天未观察到明显变化。28天后，脑前叶束呈现出明显保留的小直径和大直径轴突以及一些正在退化的中等直径轴突，其轮廓不规则，轴浆外观空洞。视神经柄切除40天后，小（I型）和中等（II型和III型）轴突均显示出部分或完全退化的迹象，但大神经纤维（IV型）仍然完整。45天后，束显示出晚期退化的迹象，除了大轴突外，几乎没有外观正常的纤维。在这最后三个时间点，退化的轴突表现出不同的电子密度和外观，这可能与该过程的不同起始时间相关。此外，细胞质中有颗粒的细胞，可能是血细胞，非常明显，尤其是在轴突切断后40天和45天。这些细胞可能在脑前叶束退化过程中与神经胶质细胞共同承担吞噬细胞碎片的功能。定量分析表明，退化纤维的数量在损伤后28天至40天显著增加，而正常纤维的数量相应减少。对正常和退化轴突横截面积的测量表明，II型和III型（中等）轴突在I型（小）轴突之前开始退化。IV型（大）轴突即使在40天后也不会退化。因此，我们可以得出结论，这些传入纤维的退化在轴突切断后开始较晚，但之后以更快的速度进行，直到小轴突和中等轴突完全退化。
