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目的:研究大鼠孕期铅暴露后子代海马突触变化与PSD-95表达改变的相关性,探讨铅暴露损伤学习记忆功能的机制。方法:通过饮用0.02%醋酸铅水溶液建立孕期铅暴露模型,利用原子吸收分光光度仪检测血铅,透射电镜技术检测海马突触密度,蛋白印记技术检测子代大鼠海马组织中VGLUT、VGAT和PSD-95的表达。结果:对照组和铅暴露组雄性21 d大鼠体重分别为(55.73±4.23)g和(56.01±5.97)g,无显著差异(P>0.05);对照组与铅暴露组雄性21 d大鼠血铅分别为(10.2±2.1)μg/L和(301.2±34.8)μg/L,血铅水平明显升高(P<0.01);对照组与铅暴露组雄性21 d大鼠单位面积突触数目分别为32.79±2.03和23.46±1.97,突触密度明显减少(P<0.01);铅暴露后,VGAT的表达量没有明显变化(P>0.05),VGLUT和PSD-95的表达量明显减少(P<0.01)。结论:PSD-95表达减少引起海马兴奋性突触数目的下降是发育期铅暴露损伤学习记忆功能的可能机制。
OBJECTIVE: To study the correlation between synaptic changes of hippocampus and the expression of PSD-95 in the offspring of pregnant rats after lead exposure and to explore the mechanism of learning and memory impairment induced by lead exposure. Methods: Lead exposure model was established by drinking aqueous solution of lead acetate (0.02%). Blood lead levels were measured by atomic absorption spectrophotometry. The synaptic density of hippocampus was detected by transmission electron microscopy. The VGLUT, VGAT and PSD- 95 expression. Results: The body weight of male 21 d rats in control group and lead exposure group were (55.73 ± 4.23) g and (56.01 ± 5.97) g respectively, with no significant difference (P> 0.05) Blood lead levels were (10.2 ± 2.1) μg / L and (301.2 ± 34.8) μg / L respectively, blood lead levels were significantly increased (P <0.01); the number of synapses per unit area (P <0.01). After exposure to lead, the expression of VGAT did not change significantly (P> 0.05) and the expression of VGLUT and PSD-95 decreased significantly (P <0.01) <0.01). Conclusion: The decrease of the number of hippocampal excitatory synapses caused by the decrease of PSD-95 expression is the possible mechanism of learning and memory impairment during lead exposure.