抄録
We examined the characteristics of cerebral ischemia-induced behavioral deficit in the passive avoidance task and the effect of minaprine and other cytoprotective drugs on passive avoidance deficit induced by cerebral ischemia in Mongolian gerbils. Severe impairment of passive avoidance was apparent when the duration of the ischemia exceeded 2 min. Histopathological ischemic neuronal damage in CA1 neurons at 7 days after occlusion was also induced when the ischemia was over 2 min. Otherwise, although cerebral ischemia was carried out at 5 min, 2 hr, 5 hr or 24 hr after the training session, the passive avoidance deficit was produced 24 hr after the training session. When the training session was carried out 24 hr before the occlusion, minaprine, which was administered 30 min before the occlusion, led to a recovery of the response latency. Pentobarbital, diazepam and ethylapovincamine improved the passive avoidance deficit induced by 5-min bilateral carotid artery occlusion. On the other hand, the passive avoidance deficit was not ameliorated by Ca++-hopantenate, nicardipine and idebenone. The hippocampal damage at 7 days after occlusion was prevented by the drugs that ameliorated the passive avoidance deficit. The relationship between passive avoidance deficit and CA1 neuronal death in the hippocampus induced by cerebral ischemia warrants further attention.
