LP-BM5白血病逆转录病毒混合物感染C57B1/6小鼠神经元变性的证据

Y Kustova, M G Espey, E G Sung, D Morse, Y Sei, A S Basile
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引用次数: 26

摘要

感染LP-BM5的小鼠会出现严重的免疫缺陷,并伴有学习和记忆缺陷、神经胶质瘤和神经递质异常。神经化学变化与兴奋毒素水平升高一致,表明受感染的小鼠可能会引起神经元损伤。虽然LP-BM5感染12周后小鼠的新皮质神经元数量没有变化,但细胞骨架蛋白的表达下降,特别是在额叶和顶叶皮层,这是由MAP2、NF-200和突触素免疫反应性显示的。相反,纹状体神经元数量减少19%。其余神经元较小,突触钮扣较少,突触素和NF-200免疫反应性降低。皮层和纹状体免疫印迹证实MAP2、NF-200和synaptophysin表达降低。最后,虽然NCAM在纹状体中的表达减少,但在皮层中的表达增加。这些结果表明lp - bm5感染小鼠维持显著的神经元损伤,这可能导致其行为缺陷。此外,皮质NCAM表达的增加表明这些小鼠活跃的突触重塑以补偿持续的兴奋毒性环境,而纹状体神经元则退化。这些同时发生的退行性和代偿性过程也可能发生在AIDS痴呆复合体(ADC)患者的大脑中,他们遭受基底神经节和大脑皮层的广泛变性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Evidence of neuronal degeneration in C57B1/6 mice infected with the LP-BM5 leukemia retrovirus mixture.

Mice infected with LP-BM5 develop a severe immunodeficiency accompanied by learning and memory deficits, gliosis, and neurotransmitter abnormalities. The neurochemical alterations are consistent with elevated excitotoxin levels, suggesting that infected mice may incur neuronal damage. Although the number of neocortical neurons was unchanged in mice 12 wk after LP-BM5 infection, the expression of cytoskeletal proteins declined, particularly in the frontal and parietal cortex as indicated by MAP2, NF-200, and synaptophysin immunoreactivity. In contrast, the number of striatal neurons decreased 19%. The remaining neurons were smaller, with fewer synaptic boutons, and showed decreased synaptophysin and NF-200, immunoreactivity. Immunoblots of cortex and striatum confirmed decreases in MAP2, NF-200 and synaptophysin expression. Finally, although NCAM expression decreased in the striatum, it increased in the cortex. These results indicate that LP-BM5-infected mice sustain significant neuronal damage, which may contribute to their behavioral deficits. Moreover, the increase in cortical NCAM expression suggests active synaptic remodeling to compensate for the persistent excitotoxic environment in these mice, whereas striatal neurons degenerate. These concurrent degenerative and compensatory processes may also occur in the brains of patients with AIDS dementia complex (ADC), who suffer extensive degeneration of the basal ganglia and cerebral cortex.

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