硫喷妥钠对大鼠前额皮层突触体谷氨酸和γ-氨基丁酸释放的影响

目的　观察硫喷妥钠对大鼠前额皮层突触体谷氨酸和γ 氨基丁酸 (GABA)Ca2 + 依赖性和Ca2 + 非依赖性释放的影响。方法　制备大鼠前额皮层粗突触体。用人工脑脊液(aCSF)孵育 ,分为 5组 :基础释放组 (Base)、硫喷妥钠 10μmol·L-1组 (THS10 )、硫喷妥钠 30 μmol·L-1组 (THS30 )、硫喷妥钠 10 0 μmol·L-1组 (THS10 0 )、硫喷妥钠 30 0 μmol·L-1组 (THS30 0 ) ,每组含 8份突触体。向每组各等份突触体反应液中加入不同浓度的硫喷妥钠 (Base组不加入 ) ,于 37℃条件下应用 30mmol·L-1KCl或 2 0 μmol·L-1veratridine诱发谷氨酸和GABA释放。应用反相高效液相色谱法 (RP HPLC)测定各反应液中的谷氨酸和GABA浓度。观察谷氨酸和GABACa2 + 非依赖性释放时 ,aCSF中不含Ca2 + 。结果　硫喷妥钠 30、10 0、30 0 μmol·L-1可显著抑制KCl或vera tridine诱发的Ca2 + 依赖性谷氨酸释放 (P <0 0 1,P <0 0 1,P <0 0 1) ,IC50 分别为 2 5 6 μmol·L-1和 2 6 3μmol·L-1;THS10与THS30组 ,THS30与THS10 0组之间差异有显著性 (P <0 0 1,P <0 0 1)。硫喷妥钠各浓度组中 ,Ca2 + 依赖性GABA释放及Ca2 + 非依赖性谷氨酸和GABA释放水平与Base组比较差异无显著性 (P >0 0 5 )。结论　硫喷妥钠可剂量依赖性地抑制大

Effect of thiopental sodium on the release of gluamate and γ-aminobutyric acid from rats prefrontal cortical synatosomes

Aim To investigate the effect of thiopental sodium on the release of glutamate and GABA from synaptosomes of rats prefrontal cortex. Methods Synaptosomes were made from rats prefrontal cortex and incubated with artificial cerebral and spinal fluid (aCSF), then divided into five groups: group base release (Base), group thiopental sodium 10 μmol·L -1 (THS 10), group thiopental sodium 30 μmol·L -1 (THS 30), group thiopen tal sodium 100 μmol·L -1 (THS 100) and group thiopental sodium 300 μmol· L -1 (THS 300). Various concentrations of thiopental sodium were added to aC SF, the release of glutamate and GABA were performed under 37℃ and measured using reversed-phase high-performance liquid chromatography (RP-HPLC). When Ca 2+-independent release of glutamate and GABA were studied, Ca 2+ was omitted from aCSF.Results Compared with Base, thiopental sodium 30 , 100 and 300 μmol·L -1 inhibited Ca 2+-dependent release of gluta mate evoked by KCl or veratridine significantly (P<0.01,P<0.01,P<0.01),but for Ca 2+-dependent release of GABA and Ca 2+-independent release of glutamate and GABA, there were no differences between the studied groups. Conclusion Thiopental sodium could inhibit Ca 2+-dependent release of glutamate from rats prefrontal cortex in a concentration-dependent manner, but had no effect on Ca 2+-dependent release of GABA and Ca 2+-independent release of glutamate and GABA.