摘要
目的研究实验性癫痫发作大鼠海马结构内一氧化氮（ＮＯ）环磷酸鸟苷（ｃＧＭＰ）信使机制及其意义。方法雄性ＳＤ大鼠４１只，随机分为对照组（５只）、红藻氨酸（ＫＡ）１０、３０、６０分钟组（每组６只）和Ｌ硝基精氨酸甲酯（ＬＮＡＭＥ）＋ＫＡ１０、３０、６０分钟组（每组６只）。用放射免疫法测定ＫＡ诱导性癫痫发作中各时点海马结构内ｃＧＭＰ含量及ＬＮＡＭＥ的干预效应。结果ＫＡ注射引起大鼠海马结构内ｃＧＭＰ浓度升高，并加重大鼠癫痫发作（湿狗样摇动提早出现和发生次数增多）；ＫＡ注射前３０分钟给予ＬＮＡＭＥ可明显抑制ＫＡ１０、３０分钟组ｃＧＭＰ浓度的升高，但ＬＮＡＭＥ对ＫＡ６０分钟组ｃＧＭＰ的抑制作用不显著。结论在ＫＡ发作早期，ｃＧＭＰ浓度升高与内源性ＮＯ有关；ＮＯ的抗发作效应可能与ｃＧＭＰ信使机制存在某种联系。
Objective To investigate the mechanism of nitric oxide (NO) cyclic guanosine monophosphate (cGMP) messenger pathway in the hippocampal formation (HF) of the rats in kainic acid (KA) induced seizures. Methods 41 rats were randomly divided into the control group (5 rats), the KA for 10, 30 and 60 min groups (6 rats for each group) and the L nitro arginine methyl ester (L NAME)+KA for 10 , 30 and 60 min groups (6 rats for each group). The concentrations of cGMP in HF in different stags during seizures were determined using radioimmunoassay and the effect of L NAME was conducted. Results We found that KA caused an apparent accumulation of cGMP in HF, but pretreatment of L NAME could significantly inhibit the cGMP level in HF 10, 30 min after KA and worsened KA seizures with earlier occurence and greater number of wet dog shakes (WDS), while no significant inhibition effect of L NAME on cGMP accumulation in HF 60 min after KA. Conclusions Our findings suggest that cGMP accumulation was related to endogenous NO during early course of KA seizures and the antiseizure action of NO was in part linked with cGMP messenger pathway.
出处
《中华神经科杂志》
CAS
CSCD
1998年第6期361-363,共3页
Chinese Journal of Neurology
