中文摘要：

为了探讨可吸入颗粒物（PM10）对神经功能损伤的突触机制,研究通过建立大鼠气管注入染毒模型,考察了不同浓度PM10暴露对突触素（SYP）、突触后致密物（PSD-95）、NMDA受体2B亚型（NR2B）、磷酸化胞外信号调节激酶（p-ERK）和环磷腺苷效应元件结合蛋白（p-Creb）表达水平的影响,并对突触超微结构进行观察。结果表明,PM10暴露增加SYP、PSD-95和NR2B的表达,上调p-ERK和p-Creb的表达水平,并呈现一定的剂量-效应关系,大鼠海马区突触超微结构的变化与上述结果相吻合,这意味着PM10暴露可能通过改变突触可塑性引起神经功能损伤。

英文摘要：

To explore the synapse mechanism of PM10 exposure induced neurotoxicity in rat brain,we treated Wistar rats with different concentrations PM10 through intratracheal instillation.Then we determined the protein expression of SYP,PSD-95,NR2 B,p-ERK and p-Creb,and observed the ultrastructural of hippocampal synapses.The results indicated that PM10 exposure increased the related protein level of synaptic plasticity,presented dose-effect relationship to a certain extent.Morever,the variation of synapses characteristics in the rat hippocampus further confirmed the above results.It suggest that PM10 exposure might cause neurotoxicity via the changes of synaptic plasticity.