红藻氨酸诱导性癫痫发作大鼠海马cNOS及iNOS的变化及作用

Changes and roles of cNOS and iNOS in rat hippocampal formation after kainic acid induced seizures

目的研究组成型一氧化氮合酶（ｃＮＯＳ）及诱导型一氧化氮合酶（ｉＮＯＳ）在红藻氨酸（ＫＡ）诱导癫痫发作中的变化及作用。方法采用免疫组织化学方法显示ｃＮＯＳ及ｉＮＯＳ的变化；Ｎｉｓｓｌ染色显示神经元的损害。结果ＫＡ３０分钟ｃＮＯＳ较对照组明显增加（Ｐ＜０．０５），随后下降至正常水平；ＫＡ诱导２小时ｉＮＯＳ明显升高，以ＣＡ１区为著，至ＫＡ６小时达高峰，然后在高水平缓慢下降；Ｎｉｓｓｌ染色神经元变性坏死ＣＡ３＝齿状回＞ＣＡ１。结论ＫＡ诱导癫痫发作导致海马ｃＮＯＳ及ｉＮＯＳ表达增多，神经元的坏死与ＮＯＳ表达增多无明显关系。

Objective To study the changes and roles of cNOS and iNOS in kainic acid(KA)induced epilepsy seizures. Methods Immunohistiochemistry and Nissl staining were performed to identify cNOS like immunoreactivity,iNOS like immunoreactivity and neuronal injury respectively. Results There was a marked increase in cNOS like immunoreactivity at 30 min after KA i.p., then it decreased to the normal level. At 2 h after KA i.p., iNOS like immunoreactivity began to increase. CA 1 region was much more pronounced at 6 h after KA i.p.,then it dropped slowly at a high level. Nissl staining neurogenic degeneration necrosis CA 3=dentate gyrus> CA 1 . Conclusion KA induced epilepsy seizures led to an increase in cNOS and iNOS immunoreactivity. The increase of NOS expression had not remarkable correlation with neuronal deaths.