Ha J H, Sei Y, Basile A S
Laboratory of Neuroscience, NIDDK, National Institutes of Health, Bethesda, Maryland 20892-0826.
J Neurochem. 1995 Apr;64(4):1896-8. doi: 10.1046/j.1471-4159.1995.64041896.x.
Mice infected with the LP-BM5 murine leukemia virus mixture develop severe immunosuppression and an encephalopathy characterized by spatial learning deficits. Twelve weeks after infection of C57BL/6J mice with LP-BM5, significant (50-60%) reductions in Met-enkephalin and substance P levels were observed in the striatum, whereas somatostatin levels were unchanged. In addition, a 39% decrease in hypothalamic substance P concentrations was observed, with no alteration in Metenkephalin levels. The apparent selectivity of the decrease in neuropeptide concentrations indicates that a functional alteration of the primary striatal efferent neurons occurs in this infection, which may contribute to the impairment of spatial learning observed in these mice. Moreover, this decrease in striatal neuropeptide levels is similar to the neuropathological changes in basal ganglia observed in HIV-infected individuals and is consistent with previous studies suggesting that the LP-BM5-infected mouse may serve as a useful model of AIDS dementia.
感染LP - BM5鼠白血病病毒混合物的小鼠会出现严重的免疫抑制和以空间学习缺陷为特征的脑病。用LP - BM5感染C57BL / 6J小鼠12周后，在纹状体中观察到甲硫氨酸脑啡肽和P物质水平显著降低（50 - 60%），而生长抑素水平未改变。此外，观察到下丘脑P物质浓度降低了39%，甲硫氨酸脑啡肽水平没有变化。神经肽浓度降低的明显选择性表明，在这种感染中，原发性纹状体传出神经元发生了功能改变，这可能导致这些小鼠出现空间学习障碍。此外，纹状体神经肽水平的这种降低与在HIV感染个体中观察到的基底神经节神经病理变化相似，并且与先前的研究一致，这些研究表明感染LP - BM5的小鼠可能是艾滋病痴呆的有用模型。
