Sterman A B
J Neuropathol Exp Neurol. 1982 Jul;41(4):400-11. doi: 10.1097/00005072-198207000-00003.
Although the neuronal cell body functions critically in maintaining and repairing the axon, little attention has been focused on the soma during neurotoxin-induced dying-back of the axon. To help elucidate changes in the perikarya during axonal dying-back, this study employed the hexacarbon model of axonal neuropathy in a setting designed to maximize the chances of detecting structural alterations. A spectrum of cell body modifications occurred in the fifth lumbar dorsal root ganglia (DRG) of rats chronically exposed to 2,5-hexanedione. These included distinctive cytoplasmic remodeling, a perineuronal cell reaction, and evidence of neuronal death with neuronophagia. These findings suggest the importance of the cell body in the pathogenesis of neurotoxin-induced axonal degeneration and imply that complex soma-axon interactions may help determine the fate of intoxicated neurons.
虽然神经元细胞体在维持和修复轴突方面起着关键作用,但在神经毒素诱导的轴突逆行性死亡过程中,人们对细胞体的关注较少。为了帮助阐明轴突逆行性死亡期间核周体的变化,本研究采用轴索性神经病的己二酮模型,该模型的设计旨在最大限度地提高检测结构改变的可能性。长期暴露于2,5-己二酮的大鼠第五腰段背根神经节(DRG)出现了一系列细胞体改变。这些改变包括独特的细胞质重塑、神经周细胞反应以及伴有噬神经元现象的神经元死亡证据。这些发现表明细胞体在神经毒素诱导的轴突变性发病机制中的重要性,并暗示复杂的细胞体-轴突相互作用可能有助于确定中毒神经元的命运。