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作 者:杨素芬[1] 杨正钦[1] 周歧新[1] 吴芹[2] 黄燮南[2] 石京山[2]
机构地区:[1]重庆医科大学药理学教研室,重庆400016 [2]贵州省遵义医学院药理学教研室,贵州遵义563003
出 处:《药学学报》2004年第4期241-244,共4页Acta Pharmaceutica Sinica
基 金:贵州省省长基金资助项目 ( 2 0 0 1 0 1 6 )
摘 要:目的 观察大鼠海马内注射 β AP2 5 - 3 5 后学习记忆行为、c fos基因表达变化及蜕皮甾酮的干预作用 ,以探讨蜕皮甾酮改善学习记忆的机制。方法 大鼠双侧海马内微注射 β AP2 5 - 3 5 10 μg ,Morriswatermaze观察其学习记忆行为 ,免疫组化SABC法观察c fos基因的表达。结果 结果显示 ,与模型组比较 ,尼莫地平组及蜕皮甾酮 (ECR)组的潜伏期缩短、搜索时间延长 ;同时模型组大鼠皮层及海马内c fos蛋白表达明显降低 ,而高剂量ECR组c fos蛋白的表达则相对增加。结论 海马内注射 β AP2 5 - 3 5 可引起大鼠空间学习记忆障碍 ,并抑制c fos的表达 ;ECR酮可改善 β AP引起的大鼠空间学习记忆障碍 ,并相对增加cAimTo observe the behavior in learning and memory and the expression of c-fos gene from the brain of rats induced by β-AP 25-35 , and the intervention of ec dysterone,in order to explore the protective mechanism of ecdysterone on the dys function of learning and memory of the rat induced by β-AP 25-35 . Methods Microinjection of β-AP 25-35 into hippocampus induced learning and memory dysfunction of rats. The learning and memory of rats were observed by M orris Water Maze. The expression of c-fos gene in the brain was detected by imm unohistochemistry. ResultsThe results of Morris Water Maze showed that after rats were microinjected β-A P 25-35 into hippocampus, the rats in model group took longer latency and s earching distance compared with the ones in control group (P<0 01), and the rats in treated group (ECR 4 mg·kg -1 , ECR 8 mg·kg -1 and nimodipin e 7 2 mg·kg -1 ) took shorter latency and searching distance, especially t he ECR 8 mg·kg -1 group (P<0 01). At the same time, after the 5 days training, there was a higher expression of c-fos in hippocampus and cortex from the rats in control group than that in model group (P<0 01), but in the tr eated group, there was a relatively higher expression of c-fos, especially the ECR 8 mg·kg -1 group (P<0 01). Conclusion Microinjection of β-AP 25-35 into the rat hippocampus resulted in dysfunc tion of learning and memory. Ecdysterone was shown to improve the learning and m emory of the rats and increase the expression of c-fos. Increasing the expressi on of c-fos is probably one of the most molecular mechanism of its protection.
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