Li Xia-Qing, Sarmento Luciana, Fu Zhen F
Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, 30602, USA.
J Virol. 2005 Aug;79(15):10063-8. doi: 10.1128/JVI.79.15.10063-10068.2005.
The structural alterations of neuronal processes in mice were investigated after the mice were infected with rabies virus (RV). Silver staining of infected brain sections showed severe destruction and disorganization of neuronal processes in mice infected with pathogenic RV but not with attenuated RV. However, neuronal bodies showed very little pathological changes. Electron microscopy revealed the disappearance of intracellular organelles, as well as the disappearance of synaptic structures and vesicles. Infection of primary neurons with pathogenic, but not attenuated, RV resulted in the destruction of neuronal processes and disappearance of microtubule-associated protein 2 and neurofilament immunoreactivity, which suggests that pathogenic RV causes degeneration of neuronal processes possibly by interrupting cytoskeletal integrity.
在小鼠感染狂犬病病毒（RV）后，对其神经元突起的结构改变进行了研究。感染脑切片的银染色显示，感染致病性RV而非减毒RV的小鼠的神经元突起出现严重破坏和紊乱。然而，神经元胞体显示出极少的病理变化。电子显微镜显示细胞内细胞器消失，以及突触结构和囊泡消失。用致病性而非减毒的RV感染原代神经元导致神经元突起破坏以及微管相关蛋白2和神经丝免疫反应性消失，这表明致病性RV可能通过破坏细胞骨架完整性导致神经元突起退化。
