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N-methyl-D-aspartate receptors(NMDAR) are glutamate gated ion channels mediating the vast majority of excitatory neurotransmission in central neural system.NR3 is recently discovered subunits of NMDAR,and has been shown to reduce the calcium permeability when is involved in NMDAR.Since Ca2+ influx through NMDAR-operated channels is considered as predominant reason to induce excitotoxicity,NR3 subunits may provide a protective role by depressing calcium overloading.In the present study,it was found that the expression of NR3A protein on rat hippocampus began to increase on the postnatal days,which reached the highest expression level on post natal day 10,and decreased gradually,which remained low into the adulthood.NR3A protein expression was increased in the models of two vessel occlusion rat brain ischemia and cell oxygen and glucose deprivation.The protective capability against ischemic injury was positively related to the expression level of NMDAR 3A on rat hippocampus slices.NR3A overexpressed cells showed higher viability than wild-type cells after cell injury.The mechanism of NR3A anti-injury ability may mainly involve in lowering intracellular Ca2+,and suppressing the generation of hydroxyl radical and NO.
N-methyl-D-aspartate receptors (NMDARs) are glutamate gated ion channels mediating the vast majority of excitatory neurotransmissions in central neural system. NR3 is recently discovered subunits of NMDAR, and has been shown to reduce the calcium permeability when is involved in NMDAR .ince Ca2 + influx through NMDAR-operated channels is considered as predominant reason to induce excitotoxicity, NR3 subunits may provide a protective role by depressing calcium overloading. In the present study, it was found that the expression of NR3A protein on rat hippocampus began to increase on the postnatal days, which reached the highest expression level on post natal day 10, and decreased gradually, which remained low into the adulthood. NR3A protein expression was increased in the models of two vessel occlusion rat brain ischemia and cell oxygen and glucose deprivation. The protective capability against ischemic injury was positively related to the expression level of NMDAR 3A on rat hippocampus slices. NR3A o verexpressed cells showed higher viability than wild-type cells after cell injury. The mechanism of NR3A anti-injury ability may mainly involve in lowering intracellular Ca2 +, and suppressing the generation of hydroxyl radical and NO.