红藻氨酸诱导癫痫发作大鼠海马NOS的表达

THE EXPRESSION OF NOS WHEN KA CAUSE EPILEPSY IN RAT HIPPOCAMPUS

目的：研究ＫＡ诱导癫痫发作对大鼠海马ＮＯＳ表达的影响；方法：采用ＮＡＤＰＨ—ｄ组织化学方法显示ＮＯＳ的变化。Ｎｉｓｓｌ染色显示神经元的变性坏死；结果：ＫＡ３０ｍｉｎ海马各区ＮＯＳ阳性细胞明显增加，以ＣＡ１、ＣＡ２区为著，ＫＡ１ｈ、２ｈ与对照无差异（Ｐ＞０．０５），以后逐渐增加，至ＫＡ６ｈＮＯＳ阳性细胞最多，然后逐渐减少。Ｎｉｓｓｌ染色神经元缺失ＣＡ３＝齿状回＞ＣＡ１区；结论：ＫＡ诱导癫痫发作引起海马ＮＯＳ表达增加，ＮＯＳ产生ＮＯ早期参与癫痫发生。

Objective:Several histologic techneques were used to study the effect of brain injury secondary to kainic acid induced seizures on the production of nitric oxide synthase (NOS).Methods:NADPH diaphorase histochemistry and Nissl staining were performed to identify cellular NADPH diaphorase activity and neuronal injury respectively.Results:There was a marked increase in NOS activity at 30min after KA i.p. Then it decreased.At 3th after KA i.p. it began to increase again.At 6h after KA i.p.,This increase was much more pronounced.Then it decreased again.KA induced seizures caused a loss of CA3=dentate hilar>CA 1 neurons.Conclusions:KA induced seizures is followed by an increase in NOS activity in the rat hippocampal formation,and this appears to be predominantly at 30min and 6h after KA i.p. An associated increase in NO may participate the generation of seizures in early stage.It has an antiepileptic function in the latter period.