【摘要】 目的观察一氧化氮(NO)在癫痫发作早期的抗发作效应及可能的细胞学机制。方法应用一氧化氮合酶(NOS)抑制剂L-硝基精氨酸(L-NNA)对红藻氨酸(KA)致痫大鼠的发作进行干预,同时用免疫组织化学染色方法观察海马结构胶质原纤维酸性蛋白(GFAP)的表达。结果KA致痫3h大鼠海马结构GFAP免疫反应性发生区域性增强改变,增强区主要为CA3-CA1锥体细胞层(p)和齿状回门区(h);L-NNA预处理组上述区域性增强改变更明显,同时致痫大鼠湿狗样摇动(WDS)的潜伏期缩短、Baran评分增加,症状加重。结论内源性NO对KA致痫大鼠GFAP的表达有影响,这可能是NO在KA致痫早期具有抗发作效应的机制之一。更多还原

【Abstract】 Objective To clarify the anticonvulsant effect of nitric oxide(NO) and its possible cytomechanisms at the early stage of seizures induced by kainic acid in rats.Methods The Epilepsy were induced by KA in Sprague-Dawley rats. Some of the rats were pretreated with nitric oxide synthase non-selective inhibitor,L-nitroarginine(L-NNA) . The changes of epileptic activity and glial fibrillary acidic protein immunoreactivity (GFAP-IR) of hippocampal astrocytes in rats were studied by immunohistochemistry methods in 3 hours.Results ①retreatment by L-NNA decreased the latency of wet dog shake(WDS) and increased Baran Score induced by KA( P<0.01 or P<0.05 ).②L-NNA alone locally decreased the number of GFAP-positive astrocytes but increased staining intensity and hypertrophy of GFAP-positive astrocytes in the dorsal hippocampus of normal rats (P<0.01 or P<0.05);KA alone locally increased the number,staining intensity,proliferation and hypertrophy of GFAP-positive astrocytes,mainly in the hilar area and stratum pyramidale.L-NNA+KA potentiated the changes of GFAP-positive astrocytes induced by KA.Conclusion These findings supported the point that NO was an endogenous antiepileptic substances.NO could influence the changes of GFAP-IR,which might be one of the cytomechanisms of nitric oxide to produce antiepileptic effects.更多还原