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.
Bibliographical noteFunding Information:
The authors would like to thank Mr. Seung Uk Lee for his technical help in this study. This work was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology ( 2012R1A1A2001404 ), and by a grant ( 2010K000823 ) from the Brain Research Center of the 21st Century Frontier Research Program funded by the Ministry of Education, Science and Technology, the Republic of Korea.
All Science Journal Classification (ASJC) codes
- Clinical Neurology