Ohno M, Yamamoto T, Watanabe S
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Brain Res. 1994 Jan 14;634(1):173-7. doi: 10.1016/0006-8993(94)90273-9.
A 5-min period of cerebral ischemia increased the number of errors in a working memory task with three-panel runway paradigm, while it had no effect on reference memory errors. The nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), infused into the bilateral dorsal hippocampus at 100 micrograms/side immediately after blood flow reperfusion, significantly reduced the increase in working memory errors expected to occur 24 h after 5 min of ischemia. Intrahippocampal administration of the inactive isomer D-NAME at 100 micrograms/side immediately after reperfusion had no effect on the increase in working memory errors in the ischemic rats. These findings suggest that the mechanism mediated by hippocampal NO synthesis during the early reperfusion phase contributes to the postischemic impairment of working memory.
5分钟的脑缺血会增加采用三板式跑道范式的工作记忆任务中的错误数量，而对参考记忆错误没有影响。在血流再灌注后立即向双侧背侧海马体注入100微克/侧的一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸甲酯（L-NAME），可显著减少预计在5分钟缺血后24小时出现的工作记忆错误增加。再灌注后立即向海马体内双侧注入100微克/侧的无活性异构体D-NAME，对缺血大鼠工作记忆错误的增加没有影响。这些发现表明，早期再灌注阶段海马体NO合成介导的机制导致了缺血后工作记忆的损伤。
