Objective    To study the role of N-methyl-D-aspartate (NMDA) receptor subunit NR2A in loss of dendritic spines in CA1 region and cognitive dysfunction due to reperfusion of cerebral ischemia.      Methods    A global cerebral ischemia model of male C57BL/6 GFP transgenic mice was established using the three-Vessel occlusion (3-VO) method. The mice were randomly divided into sham-operation group

ischemia/reperfusion (I/R) group and NVP-AAM077 treatment group (NVP). Step-down test was used to evaluate the learning and memory ability of mice. Alterations of dendritic spines in CA1 region were detected by laser scanning confocal microscopy.     Results     The learning and memory ability was significantly poorer in I/R group than in sham-operation group(P0.05). The function was significantly poorer in NVP treatment group than in sham-operation group and I/R group (P0.05). The number of dendritic spines in CA1 region was significantly less in I/R group than in shamoperation group (P0.01)

indicating that NVP can increase the loss of dendritic spines in CA1 region due to I/R injury (P0.05).      Conclusion     NMDA receptor subunit NR2A plays an important role in loss of dendritic spines and cognitive dysfunction in mice due to I/R injury.