Cerebral ischemia models were used for analysis of mechanism of neuronal cell death and/or damage.Ischemia is caused dominantly by severe hypoxia and hypoglycemia.Recently, we analyzed the effects of hypoxia alone in vivo level.After in vivo hypoxia; 5% 0 2 , 95% N 2 at 22±1 ' C fo r 30 min, neuronal damage was observed in the CA3 , hilus of dentate gyrus (hilus of DG) dentate gyrus (DG) .The CAl which vulnerable for ischemic injury was free fro m neuronal damage.In this study, we examined the effects of novel non-NMDA receptor antagonist, 2,3-Dihydroxy-6-nitro-7 -sulfamoy 1-benzo(F)quinoxaline (NBQX) against in vivo hypoxia induced neuronal damage.An administration of NBQX (30 mg/kg x 3, i.p.) at 15 and 5 min before and 10 min after 30-min hypoxia treatment, showed neuroprotective effects in the CA3 and DG after 3 and 21 days after hypoxia treatment.NBQX did not affect in the CA 1.These results suggest that hypoxia may induce neuronal damage in the CA3 and DG through activation of non-NMDA receptors.