【摘要】 为探讨一氧化氮在听源性惊厥点燃中的作用．用NADPH-d组织比学方法和体视学分析，研究厂Wistar种系的听源性惊厥易感大鼠（P77PMC）惊厥和点燃后听觉核团内NOS阳性神经元的分布及差异。结果显示：（1）P77PMC大鼠一次惊厥后，听觉核团和前脑结构内可见广泛的NOS阳性神经元，其分布类似于正常大鼠；（2）点燃后，听觉核团和前脑结构内NOS染色增深，NOS阳性神经元增加。特别是在下丘和嗅周皮质．除NOS阳性神经元明显增多外．其分布亦发生改变。本研究提示，听源性惊厥可诱导NOS表达增加，这种增加可能对于保持神经元增高的易感性有关。更多还原

【Abstract】 Kindling of audiogenic seizures is a good animal model of epilepsy and neuronal plasticity that. in contrast to naturallyoccurring epilepsy, allows study of the initial states of formation. In order to explore the role of nitric oxide (NO) in audiogenickindling, the present study investigated the distribution and difference of NOS-positive neurons in the auditory nuclei and forebrain structures after single (AS) and kindled (KAS) audiogenic seizures in P77PMC rats. a strain of Wistar audiogenic seizureprone rats. NADPH-diaphorase histochemistry was used to identify NOS-positive neurons by light microscopy. We obtained thefollowing results: (1) in AS rats. NOS-positived neurons were distributed in all of the auditory nuclei and forebrain structures.and the staining pattern of NOS was similar to previous finding observed in normal rats; (2) in KAS rats, the pattern of NOSpositive neurons was approximately similar to that in AS rats. As compared with AS rats. the density and intensity of positiveneurons significantly increased in all of the examined areas of the auditory nuclei and forebrain structures (P＜0. 05 or 0. 01). Especially. the staining pattern of NOS had a significant change in foe perirhinal cortex, and a lot of positive neurons appeared inthe deep layer of this cortex. These results indicated that audiogenic kindling could increase NOS expression. and the increasedexpression of NOS might play a role in sustaining the increased neuronal susceptivity.更多还原