Nitta A, Fukuta T, Hasegawa T, Nabeshima T
Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University School of Medicine, Tsuruma-cho, Showa-ku, Japan.
Jpn J Pharmacol. 1997 Jan;73(1):51-7. doi: 10.1254/jjp.73.51.
To investigate the toxicity of beta-amyloid protein, a component of the senile plaques in Alzheimer's disease, it was infused into the cerebral ventricle of rats for 14 days by a mini-osmotic pump. Performances in the water maze and passive avoidance tasks in beta-amyloid protein-treated rats were impaired. Choline acetyltransferase activity significantly decreased in the hippocampus both immediately and 2 weeks after the cessation of the infusion. However, the learning impairment was recoverable 2 weeks after cessation of the infusion. Both immediately and 2 weeks after the cessation of the infusion, glial fibrillary acidic protein immunoreactivity increased. Furthermore, beta-amyloid protein altered the staining in the nuclei of hippocampal cells for only 2 weeks after the cessation. These results suggest that beta-amyloid protein produces some damage in the central nervous system in vivo.
为研究阿尔茨海默病老年斑成分β-淀粉样蛋白的毒性，通过微型渗透泵将其注入大鼠脑室14天。接受β-淀粉样蛋白处理的大鼠在水迷宫和被动回避任务中的表现受损。输注停止后即刻及2周时，海马中的胆碱乙酰转移酶活性显著降低。然而，输注停止2周后学习障碍可恢复。输注停止后即刻及2周时，胶质纤维酸性蛋白免疫反应性均增加。此外，β-淀粉样蛋白仅在输注停止后的2周内改变海马细胞核的染色。这些结果表明，β-淀粉样蛋白在体内对中枢神经系统产生了一些损害。
