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目的:观察慢性氟中毒大鼠脑组织中磷酸化-N-甲基-D-天冬氨酸受体（phosphorylated N-methyl-D-aspartat receptor，P-NMDAR）亚基及钙调蛋白依赖性蛋白激酶Ⅱ（calmodulin-dependent kinaseⅡ，CaMKⅡ）蛋白表达变化，探讨慢性氟中毒神经损伤的分子发病机制。方法:选择1月龄SD大鼠18只（雌雄各半），适应性喂养1周，按体质量[（100 ± 20）g]采用随机数字表法分为对照组（饮用自来水，含氟量 0.05）。免疫组化结果显示，高氟组大鼠脑组织P-NMDAR1、P-NMDAR2A、CaMKⅡ蛋白表达水平（0.026 3 ± 0.005 7、0.086 3 ± 0.009 0、0.210 9 ± 0.048 7）与对照组（0.011 8 ± 0.006 5、0.065 6 ± 0.011 1、0.143 8 ± 0.029 9）和低氟组（0.017 2 ± 0.006 8、0.062 6 ± 0.017 8、0.135 6 ± 0.029 6）比较显著升高（ n P均< 0.05），且低氟组P-NMDAR1蛋白表达水平明显高于对照组（n P < 0.05）。n 结论:长期过量氟摄入可导致大鼠神经细胞损伤，其损伤机制可能与NMDAR亚基过度激活所致的钙离子（Can 2+）超载诱导的兴奋性神经毒性有关。n “,”Objective:To observe the changes of phosphorylated N-methyl-D-aspartate receptor (P-NMDAR) subunit and calmodulin-dependent protein kinase Ⅱ (CaMK Ⅱ) protein expression in the brain tissue of rats with chronic fluorosis, and to explore the molecular pathogenesis of chronic fluorosis nerve injury.Methods:Eighteen one-month-old SD rats (half male and half female), weighing (100 ± 20) g, were randomly divided into three groups after adaptive feeding for 1 week: control group (drinking tap water, fluoride content 0.05). Compared with the control group (0.011 8 ± 0.006 5, 0.065 6 ± 0.011 1, 0.143 8 ± 0.029 9) and low fluoride group (0.017 2 ± 0.006 8, 0.062 6 ± 0.017 8, 0.135 6 ± 0.029 6), the protein expressions of P-NMDAR1, P-NMDAR2A and CaMK Ⅱ in high fluoride group were significantly increased (0.026 3 ± 0.005 7, 0.086 3 ± 0.009 0, 0.210 9 ± 0.048 7, n P < 0.05); and the protein expression of P-NMDAR1 in low fluoride group was higher than that in the control group ( n P < 0.05).n Conclusion:Long-term excessive fluoride intake can lead to nerve cell injury in rats, and the mechanism of injury maybe related to the excitotoxicity induced by calcium ion (Can 2+) overload caused by overactivation of NMDAR subunits.n