Effects of huperzine A on nucleus basalis magnocellular is lesion-induced spatial working memory deficit

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：采用八臂迷宫延迟插板的程序研究空间记忆．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·ｋｇ－１实验前３０ｍｉｎｉｐ）改善这种空间记忆障碍．毒扁豆碱（０２－０３ｍｇ·ｋｇ－１实验前２０ｍｉｎｉｐ）也有改善作用．结论：完整的ＮＢＭ是空间记忆形成的关键．石杉碱甲有效的改善ＮＢＭ损毁导致的空间记忆障碍．

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 acetyl CoA to ACh . RESULTS: Unilateral NBM lesion by kainic acid 0 02 μmol 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 ip 30 min before testing) ameliorated this spatial working memory impairment. Physostigmine (0 2-0 3 mg·kg -1 ip 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.