十溴联苯醚（PBDE-209）是近年我国环境中及人体中增加较快的环境持久性有机污染物，在流行病学研究及动物实验中已证实围生期暴露于PBDE-209后可引起子代学习、记忆能力下降。但具体机制仍不清楚。而NO/cGMP/PKGI通道在维持神经细胞正常功能及形成记忆等认知能力中起着重要的作用。基于本研究小组的前期研究结果，提出PBDE-209可能通过NO/cGMP通道，从而影响PKGI蛋白对下游调控子的调控，最终导致神经细胞表型改变的假设，利用母源性暴露PBDE-209的大鼠动物模型及体外原代培养神经细胞模型，并应用荧光共振能量转移（FRET）的新技术在活细胞上，研究围生期暴露于PBDE-209对子代神经发育异常的影响，寻找PBDE-209神经毒性的关节点，为制定如何干预及预防PBDE-209对神经发育影响提供可靠的科学依据，为国家制定相关环境保护及监测制度提供理论基础。

Recent years the content of PBDE-209 were increasing in environment and in human body in China. Epidemiologic studies and animal studies indicate prenatal and postnatal PBDE-209 exposure exhibited abnormal neurodevelopment, particularly in the domains of locomotor activity and cognitive behavior. But how PBDE-209 induced abnormal neurodevelopment was not unknown now. NO/cGMP/PKGI signaling is an important signaling in central nervous system, regulating neuronal survival, proliferation, and differentiation and paying an important role in cognitive product. Based on our previous studies, our hypothesis was PBDE-209 disrupted neuronal cell phenotype by modulating NO/cGMP/PKGI signaling. We will perform these experiments not only by using the traditional experimental technique in vitro and in vivo, but also by using fluorescence resonance energy transfet(FRET) in living cells. From these studies, we want to know the mechanism of PBDE-209 potential neurotoxicity, which can help us to prevent the effect of PBDE-209 neurotoxicity.