以往研究发现，产前应激（PS）导致的子代空间学习记忆能力下降与海马损伤有关。最近有报道称PS可以损害关联性条件化恐惧（CFC）的形成。动物通过CFC感知外界，有利于物种的生存和延续。产前应激是如何损伤子代CFC的形成？本研究拟通过改变Npas4基因在海马CA3区锥体细胞的转录和表达，观察Npas4对产前应激子代的关联性条件化恐惧形成的调控作用。首先采用产前束缚应激大鼠模型，结合CFC，观察海马CA3区锥体细胞顶树突棘密度和形态；然后记录海马CA3区的突触后电流、长时程增强和强直后增强；检测海马CA3区Npas4基因的转录和表达，相关的即刻早期基因的转录和表达，以及不同脑区谷氨酸和γ-氨基丁酸受体的表达和活性；并将Npas4基因转入海马CA3区锥体细胞，上调其表达，观察上述指标的改变。本研究将明确产前应激对子代联合型学习损伤的机制，将为临床寻求早期干预提供理论依据和新措施。

In previous studies, we found that impairment of spatial learning and memory in rat offspring induced by prenatal stress(PS)were associated with hippocampal damage. Recently, there was a report that PS could impair the formation of contextual fear conditioning(CFC). To species's survival and continuity, the formation of contextual fear conditioning(CFC) is very important that animals can apperceive environments. How does PS impair the formation of CFC in offspring? In this study, we observe the regulation of Npas4 gene in the formation of CFC in offspring by altering the transcription and expression of Npas4 gene of pyramidal neurons in hippocampal CA3 region. Firstly, we examine the formation of CFC on offspring in the model of prenatal-stress rats. Secondly, we obsevrve the density and shapes of apital dentritic spine in pyramidal neurons, record the postsynaptic currents, long-term potentiation and post tetanic potentiation in the hippocampal CA3 region of rat offspring. Thirdly, we measure the transcription and expression of Npas4 gene and associated immediate early genes in hippocampal CA3 region. we also examine the expression and activity of glutamate and γ-GABA receptors in different brain areas. Forthly, by transfecting Npas4 gene into pyramidal neurons in hippocampal CA3 region, we observe the role of Npas4 overexpression in above items. This study try to disclose the mechanism of impairment of associative learning in prenatal-stress offspring and offer new insights to improve the poor ability of associative learning in prenatal-stress offspring.