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目的 探讨内源性一氧化氮(NO)参与癫痫发作机制。方法 用分光光度法检测红藻氨酸(KA)诱导性癫痫发作大鼠海马结构、杏仁核内NO合酶(NOS)活性的早期变化。结果 发现注射KA(15mg/kg)后10min和30min海马结构内NOS活性升高(P<0.05);注射KA后30min杏仁核内NOS活性升高(P<0.05);注射KA60min后海马结构和杏仁核内NOS活性均下降。KA全身给药引起海马结构内NOS活性很快升高,继之杏仁核内NOS活性升高。结论 KA毒性直接导致海马结构神经细胞活性增强,并激活其中的NOS,参与大鼠癫痫发作的始动过程及传播过程。
Objective To investigate the mechanism of endogenous nitric oxide (NO) involved in seizure. Methods The early changes of NO synthase (NOS) activity in hippocampal formation and amygdala were detected by spectrophotometry in kainate induced seizure rats. The results showed that the activity of NOS in the hippocampus was increased at 10 and 30 minutes after injection of KA (P <0.05), and the activity of NOS in amygdala increased 30 minutes after injection of KA (P <0.05) Nuclear NOS activity decreased. Systemic administration of KA causes a rapid increase in NOS activity in the hippocampal formation, followed by an increase in NOS activity in the amygdala. Conclusions KA toxicity directly leads to increased activity of hippocampal neurons and activation of NOS, which is involved in the process of start-up and transmission of seizures in rats.