Kojima Daisuke, Park Chun-Ho, Tsujikawa Shintarou, Kohara Keiko, Hatai Hitoshi, Oyamada Toshifumi, Noguchi Akira, Inoue Satoshi
Department of Veterinary Pathology, School of Veterinary Medicine, Kitasato University, Aomori, Japan.
J Vet Med Sci. 2010 Aug;72(8):1011-6. doi: 10.1292/jvms.09-0550. Epub 2010 Mar 25.
BALB/c mice were inoculated intracerebrally with fixed rabies virus (CVS-11) and pathomorphological changes in the central nervous system were studied. Infected mice showed ruffled hair, hunchback, anorexia, emaciation and ataxia at 5 days postinoculation (DPI), but paralysis did not occur. Viral antigens were first detected in the pyramidal cells of the cerebral cortex and hippocampus at 3 DPI, and these cells exhibited apoptosis at 5 DPI. Microglial cells and astroglial cells significantly increased in the areas of the nerve cells which showed apoptosis. However, spinal neurons and spinal dorsal root ganglion cells did not exhibit apoptosis despite virus infection. These observations indicate that different mechanism which causes apoptosis exists among the neurons of the brain and spinal cord, and glial cells play an important role in pathogenesis of the experimental rabies.
将BALB/c小鼠脑内接种固定化狂犬病病毒(CVS-11),并研究其中枢神经系统的病理形态学变化。接种后5天(DPI),感染小鼠出现毛发蓬松、驼背、厌食、消瘦和共济失调,但未发生麻痹。在3 DPI时首次在大脑皮层和海马的锥体细胞中检测到病毒抗原,这些细胞在5 DPI时出现凋亡。在显示凋亡的神经细胞区域,小胶质细胞和星形胶质细胞显著增加。然而,尽管受到病毒感染,脊髓神经元和脊髓背根神经节细胞并未出现凋亡。这些观察结果表明,脑和脊髓神经元之间存在导致凋亡的不同机制,并且胶质细胞在实验性狂犬病的发病机制中起重要作用。