nnz - 2591,一个新颖的二酮哌嗪,阻止scopolamine-induced急性成年大鼠记忆障碍。

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张关J R, Dale-Gandar L,哈吉金森年代,维氏MH

nnz - 2591,一个新颖的二酮哌嗪,阻止scopolamine-induced急性成年大鼠记忆障碍。

Behav大脑研究》2010年7月11日,210 (2):221 - 8。doi: 10.1016 / j.bbr.2010.02.039。Epub 2010年2月25日。

PubMed ID

20188767 (在PubMed

]

文摘

在老鼠,cyclo-L-glycyl-L-2-allylproline (nnz - 2591),二酮哌嗪,缺血性脑损伤后神经保护和改善运动机能在帕金森病大鼠模型。鉴于益智药二酮哌嗪的行动,我们调查的影响和潜在的作用,乙酰胆碱神经传递nnz - 2591年在大鼠空间记忆scopolamine-induced失忆后。成年雄性Wistar鼠被分配到四组:生理盐水/水;生理盐水/ nnz - 2591;莨菪碱/水和莨菪碱/ nnz - 2591。莫里斯水迷宫(微波加工)任务被用来确定空间学习和记忆。三十分钟前每天的四个采集试验,大鼠腹腔内注射(0.5毫克/公斤)东莨菪碱或盐。要么nnz - 2591(30毫克/公斤)或水的口服药物(填喂法)10分钟后注入。收购完成后第四天试验空间探测试验。免疫组织化学分析的大脑被收集。 Scopolamine impaired spatial learning and memory compared to saline treated group, particularly in the day 1 acquisition trial. NNZ-2591 did not reverse this deficit, however it significantly improved memory retention by showing more time spent in the correct quadrant. NNZ-2591 also counteracted the scopolamine-induced up-regulation of choline-acetyltransferase positive neurons in the striatum and similarly counteracted the increased synaptophysin density in the hippocampus. Furthermore, a scopolamine-independent antagonistic effect on muscarinic M2 acetylcholine receptors was found after NNZ-2591 treatment, supporting its modulation of acetylcholine neurotransmission. The data suggest that NNZ-2591 prevents scopolamine-induced acute impairment in memory and modulation of acetylcholine neurotransmission may be the mode of action underlying the memory improvement.

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药物

nnz - 2591