中文摘要：

目的观察饮水砷暴露后大鼠海马超微结构和N-甲基-D-天冬氨酸受体（NMDAR）亚基mRNA表达的变化，探讨砷致学习记忆损害的分子机制。方法将48只雄性健康断乳SD大鼠随机分为4组，每组12只。对照组饮用自来水，砷暴露组分别饮用2．72，13．6和68mg／L亚砷酸钠溶液。饲养3个月后，测定脑砷，用透射电镜观察海马超微结构，用RT—PCR检测海马组织NMDA受体亚基mRNA表达。结果脑砷值随饮水砷浓度升高而升高，13．6和68mg／L组与对照组相比，差异有统计学意义（P〈0．05）。电镜下，染砷组大鼠海马神经细胞肿胀，线粒体肿胀，脊减少或无脊，粗面内质网扩张，血管内皮细胞肿胀。与对照组相比，各砷暴露组NR2AmRNA表达量明显降低（P〈0．05）。结论大鼠砷暴露可致海马神经细胞和血管内皮细胞的损伤，降低NR2AmRNA表达量，进而可能影响学习记忆功能。

英文摘要：

Objective To investigate NMDAR subunit mRNA expression and ultrastructural changes in hippocampus of rats after exposed to arsenic. Methods Weaned SD rats were divided into four groups randomly and each group had 12 rats. The control group drank tap water, the other three groups drank 2.72 mg/L, 13.6 mg/L and 68 mg/L solution of sodium arsenite for 3 months. The arsenic levels of brain were assessed, the ultrastructual changes of rat hippocampus were observed with transmission electron microscope, and the expressions of NMDAR subunit mRNA were detected with RT - PCR. Results Arsenic concentration in brain of 13.6 mg/L and 68 mg/L groups were significantly higher than that of in control rats （P 〈0.05）. The ultrastructures of hippocampus neuron cells in arsenic exposed rats presented a series of pathologic changes. The level of NR2A mRNA was downregulated. Conclusion Exposed to arsenic can damage neuron cells and vascular endothelial cells in hippocampus of rats, and downregulate the level of NR2A mRNA.