Abstract: 【Objective】 To explore the possible mechanism of learning and memory impairment in filial rats with lead exposure of mother pregnant rats by observing the ultrastructural pathologic changes of hippocampal neurons and organelles, and the features of synaptic morphological parameters. 【Methods】 Female pregnant Spraque-Dawley (SD) rats were divided into high dose lead exposure group(HG) and low dose lead exposure group(LG) by drinking 0.1% or 0.2% lead acetate dissolved by three distilled water,the normal control group(NG) pregnant rats drank three distilled water.36 days after birth, transmission electron microscope were used to examine the ultrastructural pathologic changes of neurons and organelles,and the features of synaptic morphological parameters of hippocampal CA1 area in 9~12 male filial rats from HG,LG or NG group. 【Results】 Severe ultrastructural pathologic changes were found in hippocampal CA1 area of filial rats with lead exposure of mother pregnant rats.The changes of neuronal degeneration and necrosis,mitochondria swelling,polyribosomes disaggregation from endoplasmic reticulum,and golgiosomes dilation in lead exposure group were more significantly severe than those of the control group(P<0.05 or <0.01).Compared with the control groups, lead exposure group showed significant decreases of postsynaptic density thickness,synaptic active zone length,and synaptic interface curvature,as well as significant increases of synaptic cleft (all P<0.01) .In addition, lead exposure group showed no significant differences in synaptic numeric density and synaptic surface density as compared with the control groups. 【Conclusions】 Lead exposure of pregnant rat could result in severe ultrastructural pathologic chandes of neurons and organells,as well as the significant synaptic plasticity in hippocampal areas of filial rats.The possible mechanism of learning and memory impairment in filial rats with lead exposure of mother pregnant rats is also relative to these pathologic changes.

Key words: lead exposure, ultrastructure, hippocampus, synapse, rat

摘要： 【目的】 观察孕期铅暴露对子代大鼠脑海马区神经元、细胞器超微结构及神经突触形态学参数变化,探讨孕期铅暴露对子代大鼠学习记忆损害的可能机制。 【方法】 通过孕鼠自由饮用0.1%及0.2%醋酸铅溶液的方法建立模型,其雄性子代分别为低剂量铅暴露组(LG)及高剂量铅暴露组(HG),同时设立正常对照组(NG),每组9~12只大鼠。子代大鼠出生后36日龄应用透射电镜分别观察海马CA1区神经元、细胞器的病理超微结构改变和神经突触参数变化特征。 【结果】 铅暴露仔鼠脑海马区出现显著病理超微结构改变。HG组在神经元变性坏死、线粒体肿胀、内质网脱颗粒及高尔基体扩张等方面较对照组程度严重,差异有高度统计学意义(P<0.05或<0.01)。三组在突触后致密物质厚度、突触活性带长度、突触界面曲率及突触间隙等方面的差异有高度统计学意义(P均<0.01),提示铅暴露仔鼠脑海马CA1区突触后致密物质厚度减小、突触活性带长度缩短、突触界面曲率下降及突触间隙增宽。铅暴露组与对照组在突触数密度及面密度方面差异无统计学意义(P均>0.05)。 【结论】 孕期铅暴露可导致子代大鼠脑海马区严重的神经元和细胞器超微病理改变,同时伴有神经突触可塑性变化,推测孕期铅暴露对子代学习记忆的损害与以上病理改变有关。

关键词: 铅暴露, 超微结构, 海马, 突触 , 大鼠