Young gerbils are much more resistant to transient cerebral ischemia than the adult. In the present study, we observed that about 90% of CA1 pyramidal cells in the adult hippocampus died 4 days post-ischemia; however, about 56% of them in the young hippocampus died at 7 days post-ischemia. To compare excitotoxicity between them, we carried out immunoreactivities of NMDA receptor 1 (NMDAR1) and NMDAR2A/B in the hippocampal CA1 region (CA1) induced by 5 min of transient cerebral ischemia in the young and adult gerbils. Their immunoreactivities and protein levels in the young sham-group were much lower than those in the adult sham-group. Four days after ischemia-reperfusion, they were significantly decreased in the adult ischemia-group; however, in the young ischemia-group, they were much higher than those in the adult. Seven days after ischemia-reperfusion, NMDAR1 immunoreactivity and its level in the young were much higher than those in the adult; NMDAR2A/B immunoreactivity and its level in the young were lower than in the adult. In brief, the immunoreactivities of NMDARs were not decreased in the ischemic CA1 region of the young 4 days after transient cerebral ischemia. This finding indicates that longer maintenance of NMDARs may contribute to less and more delayed neuronal death/damage in the young CA1.
All Science Journal Classification (ASJC) codes
- Clinical Neurology