POSTISCHEMIC CHANGES OF [H-3]NIMODIPINE AND [H-3]RYANODINE BINDING INTHE GERBIL STRIATUM AND HIPPOCAMPUS

Sequential alterations of [H-3]nimodipine and [H-3]ryanodine binding i n gerbils were investigated in selectively vulnerable regions, such as the striatum and hippocampus, 1 h to 7 days after 10 min of transient cerebral ischemia. [H-3]Nimodipine binding showed no significant chan ges in the striatum and hippocampus up to 48 h after ischemia. Seven d ays after ischemia, however, a severe reduction in [H-3]nimodipine bin ding was observed in the dorsolateral striatum, hippocampal CA1 (strat um oriens, stratum pyramidale and stratum radiatum) and hippocampal CA 3 sector. On the other hand, [H-3]ryanodine binding showed a significa nt increase in the hippocampus 1 h after ischemia. Five hours after is chemia, a significant reduction in [H-3]ryanodine binding was observed only in the hippocampal CA1 sector. Thereafter, the striatum and hipp ocampus showed no significant alterations in [H-3]ryanodine binding up to 48 h after ischemia. After 7 days, a marked reduction in [H-3]ryan odine binding was observed in the striatum and hippocampus which were particularly vulnerable to ischemia. These results demonstrate that po stischemic alteration in [H-3]nimodipine and [H-3]ryanodine binding is produced with different processes in the hippocampus. They also sugge st that the mechanism for striatal cell damage caused by transient cer ebral ischemia may, at least in part, differ from that for hippocampal neuronal damage. Furthermore, our findings suggest that abnormal calc ium release from intracellular stores may play a pivotal role in the d amage. development of hippocampal neuronal. (C) 1998 Rapid Science Ltd .