石杉碱甲对基底核大细胞部损毁所致工作记忆障碍的影响

目的：研究石杉碱甲对基底核大细胞部（ＮＢＭ）损毁诱导的工作记忆障碍的影响。方法：采用八臂迷宫延迟板程序研究空间记忆。胆碱乙酰转移酶（ＣｈＡＴ）活力测定采用［＾３Ｈ］乙酰辅酶Ａ转变成［＾３Ｈ］乙酰胆碱的方法。结果：单侧损毁ＮＢＭ（卡因酸０．０２μｍｏｌ）导致空间记忆障碍。在不同的延迟间隔，大鼠完成程序产生的正确数减少和错误数增多。损毁侧大脑皮层ＣｈＡＴ酶的含量下降了大约４０％。石杉碱甲（０．２ｍｇ·

Effects of huperzine A on nucleus basalis magnocellularis lesion-induced spatial working memory deficit.

AIM: To study the effects of huperzine A on nucleus basalis magnocellularis (NBM) lesion-induced spatial working memory impairment. METHODS: A delayed-non-match-to-sample radial arm maze task was used to study spatial working memory. The choline acetyltransferase (ChAT) activity was determined by the conversion of 3H]acetyl-CoA to 3H]ACh. RESULTS: Unilateral NBM lesion by kainic acid 0.02 mumol impaired rat's ability to perform this working memory task as evidenced by fewer correct choices after different delay intervals and more total errors to complete the task. This behavioral impairment associated with a decrease in the activity of ChAT by about 40% in the ipsilateral cerebral cortex. Huperzine A (0.2 mg.kg-1 i.p. 30 min before testing) ameliorated this spatial working memory impairment. Physostigmine (0.2-0.3 mg.kg-1 i.p. 20 min before testing) also attenuated the NBM lesion-induced memory deficit. CONCLUSION: The integrity of NBM is critical for spatial working memory processing, and this working memory impairment induced by NBM lesion can be ameliorated by huperzine A and physostigmine.