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选择性M1激动剂AF102B改善啮齿动物的实验性失忆(被动回避失败)。

Amelioration of experimental amnesia (passive avoidance failure) in rodents by the selective M1 agonist AF102B.

作者信息

Nakahara N, Iga Y, Mizobe F, Kawanishi G

机构信息

Research Institute of Life Science, Snow Brand Milk Products Co., Ltd., Tochigi, Japan.

出版信息

Jpn J Pharmacol. 1988 Dec;48(4):502-6. doi: 10.1254/jjp.48.502.

Abstract

Effect of AF102B (cis-2-methylspiro-(1,3-oxathiolane-5,3')-quinuclidine) on experimental amnesia was examined using a passive avoidance task in rodents. The amnesia was produced by anti-cholinergic agents, AF64A (intracerebroventricularly) and scopolamine (subcutaneously). AF102B ameliorated the memory deficits in AF64A-treated rats at 0.1-1 mg/kg, i.p. and at 1-5 mg/kg p.o. and in scopolamine-treated mice at 1-10 mg/kg, i.p. These results suggest that AF102B may compensate for central cholinergic defects and could be developed as a possible therapeutic drug for senile dementia of the Alzheimer type.

摘要

使用啮齿动物的被动回避任务研究了AF102B(顺式-2-甲基螺-(1,3-氧硫杂环戊烷-5,3')-奎宁环)对实验性失忆的影响。失忆由抗胆碱能药物AF64A(脑室内注射)和东莨菪碱(皮下注射)诱导产生。AF102B能改善经AF64A处理的大鼠(腹腔注射剂量为0.1-1mg/kg以及口服剂量为1-5mg/kg)和经东莨菪碱处理的小鼠(腹腔注射剂量为1-10mg/kg)的记忆缺陷。这些结果表明,AF102B可能弥补中枢胆碱能缺陷,有望开发成为一种治疗阿尔茨海默型老年痴呆症的潜在治疗药物。

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