孕期人巨细胞病毒母婴垂直传播危害极大，是导致新生儿CID和出生后智力障碍的最主要原因之一。课题组前期研究证实：HCMV先天性感染导致学习记忆功能障碍与钙超载及突触性特性的改变有关，其发生机制可能与病毒和神经细胞DNA整合，干扰海马突触可塑性相关信号转导通路。本研究通过建立HCMV先天性感染的子代大鼠模型，采用在位电生理技术、原位杂交、免疫组化法分析、Western Blot和RT-PCR等方法，重点探讨HCMV先天性感染后cAMP-CREB、Ras／ERK信号转导通路的功能变化与突触可塑性、记忆相关即早基因和蛋白表达异常之间的关系。同时应用场发高分辨冷冻扫描电镜技术检测皮层、海马的微观动态损伤情况；阐明HCMV先天性感染突触可塑性损伤的信号转导机制，对防治先天性宫内感染导致的智力障碍具有重要的临床意义。

Human cytomegalovirus (HCMV) vertical transmission hurts the chilldren greatly, it is considered as the most common cause of neonatal cytomegalic inclusion disease (CID) and mental disorder. Our preliminary researchs confirmed that HCMV congenital infection damages the function of learning and memory through overloading the the level of intracellular celluar calcium and decreasing the level of synaptic properties. The main mechanism of it is that HCMV integrates into the nerve cell DNA, then interrupts the signal transduction pathways of synaptic plasticity on hippocampaus. In this study, electrophysiological techniques, situ hybridization, immunohistochemical analysis, Western Blot and RT-PCR methods are used to mainly reveal the relationship among the changes of cAMP-CREB, Ras / ERK signal transduction pathway, the lelvel of synaptic plasticity, the expression level of memory related to immediate early gene and protein thirough build a HCMV congenital infection rat model. At the same time, field emission scanning electron microscope techniques are utlilted to detect the damage of cerebral cortex and hippocampalus. Clarified the mechanisms of HCMV congenital infection injuring Synaptic plasticity by the way of signal transduction is an important clinical significance to reveal on the etiology of mental disorders。