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运用FOS免疫组化结合NADPH－d组化双重标记技术，研究了soman诱发惊厥大鼠杏仁核内c－fos高表达神经元与NADPH－d阳性神经元之间的关系。结果显示：在soman诱发惊厥后的1．5h至48h，杏仁核簇内c－fos呈现持续过度表达、FOS免疫阳性神经元的分布具有显著的亚核定位特征。NADPH－d活性在惊厥后明显增强。有10％的FOS阳性神经元同时也呈现NADPH－d阳性。而几乎所有的NADPH－d阳性神经元均呈FOS染色阳性。鉴于FOS表达的诱导和NADPH－d的激活具有共同的上游事件，即NMDA介导的钙内流，可以认为FOS引发的目的基因表达及NO的神经毒作用可能存在于杏仁核的神经元损伤机制中。
The relationship between c-fos overexpression neurons and NADPH-d positive neurons in the amygdala induced by soman in soman-induced seizures was studied by FOS immunohistochemistry combined with NADPH-d histochemical double labeling. The results showed that the expression of c-fos in the amygdala cluster continued to overexpress in 1.5h to 48h after soman-induced seizures, and the distribution of FOS-immunoreactive neurons showed significant subnuclear localization. NADPH-d activity increased significantly after convulsion. Ten percent of FOS-positive neurons also showed NADPH-d positivity. Almost all NADPH-d positive neurons showed positive FOS staining. In view of the common upstream events of induction of FOS expression and activation of NADPH-d, namely NMDA-mediated calcium influx, it can be considered that FOS-induced gene expression and NO neurotoxicity may be present in the amygdala neuronal damage mechanism in.