γ-羟基丁酸诱导性大鼠失神发作持续状态丘脑nNOS的表达及丙戊酸干预的研究

Investigation lf thalamus nNOS expression and valproic acid intervention on absence seizures induced by γ butyrolactone in rat

目的 :探索失神发作中的一氧化氮机制。方法 :用 n NOS抗体免疫组织化学法在γ-羟基酸诱导性大鼠失神发作模型上 ,对丘脑 n NOS的表达分布、动态演变过程以及丙戊酸对 n NOS表达的影响进行了观察和探讨。结果 :在正常大鼠丘脑内即固有存在 n NOS,γ-羟丁内酯注射 1 0 min时 ,丘脑内 n NOS表达即达高峰 ,6 0 min表达减少 ,预先使用丙戊酸后 ,大鼠失神发作持续时间明显缩短 ,丘脑内 n NOS表达明显减少。结论 :提示内源性一氧化氮在癫痫失神发作中起参与或调控作用 ,丙戊酸的抗痫性可能与影响脑内一氧化氮水平有关。

Objective:To study NO mechanisms in absence seizures.Methods:The expression distribution and developmental changes of nNOS were examined using immunohistochemical in the SD rat brain following systemic administration of γ butyrolactone (GHB),and the effect of valproic acid (VPA) on the GHB induced expression of the nNOS was investigated.Results:The nNOS was expressed less constitutively in the thalamus of normal rat ,the induction of nNOS reached peak at 10 min in the thalamus,began to decrease at 60 min.Prior interference with VPA reduced the developmint of GHB induced absence seizures and the expression nNOS in thalamic areas.Conclusions:The endogenous NO might play an important role in the process and VPA action might be mediated by regulating the NO in the brain.