Ohno M, Yamamoto T, Ueki S
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Eur J Pharmacol. 1991 Feb 14;193(3):357-61. doi: 10.1016/0014-2999(91)90151-f.
The effect of U-50,488H, a selective kappa-receptor agonist, on memory functions in an animal model of cerebral ischemia was investigated by use of a three-panel runway task. A 5-min period of ischemia caused a significant increase in the number of errors (pushes made on the two incorrect panels of the three panel-gates at four choice points) in a working memory task but it did not impair a reference memory task. U-50,488H at 10 and 32 mg/kg, administered i.p. immediately after blood flow restoration significantly reduced the increase in errors expected to occur in a working memory task assessed 24 h after 5 min of ischemia. This protective effect of U-50,488H on amnesia in the ischemic rat was antagonized by the kappa-receptor antagonist, MR-2266. We conclude that U-50,488H prevents the impairment of working memory following transient forebrain ischemia, an event mediated by the activation of the kappa-opioid receptor.
通过使用三面板跑道任务，研究了选择性κ受体激动剂U - 50,488H对脑缺血动物模型记忆功能的影响。5分钟的缺血期导致工作记忆任务中的错误数量（在四个选择点对三面板门的两个错误面板进行的推动）显著增加，但并未损害参考记忆任务。在血流恢复后立即腹腔注射10和32mg/kg的U - 50,488H，可显著减少预计在缺血5分钟后24小时评估的工作记忆任务中出现的错误增加。κ受体拮抗剂MR - 2266拮抗了U - 50,488H对缺血大鼠失忆症的这种保护作用。我们得出结论，U - 50,488H可预防短暂性前脑缺血后工作记忆的损害，这一事件是由κ阿片受体的激活介导的。
