摘要
目的 观察硫喷妥钠对大鼠前额皮层突触体谷氨酸释放的影响以及γ-氨基丁酸受体(GABA_A)在其中的作用。方法 SD大鼠断头取脑,分离前额皮层,加入到冰冷蔗糖溶液中进行匀浆,在0℃～4℃下以1000g离心5min,取上清液再以12000g离心20min,所得沉淀为粗突触体,用人工脑脊液孵育。分为5组:对照组(C组)、硫喷妥钠10μmol/L组(THS10组)、硫喷妥钠30μmol/L组(THS30组)、硫喷妥钠100μmol/L组(THS100组)、硫喷妥钠300μmol/L组(THS300组),每组含8份突触体。向各组人工脑脊液中分别加入10～300μmol/L不同浓度的硫喷妥钠(C组中不加入),于37℃水浴中自发释放或应用30mmol/LKCl诱发释放谷氨酸,应用高效液相色谱法测定反应液中谷氨酸含量,于水浴前向人工脑脊液中加入0.1mmol/L的荷包牡丹碱,观察其对硫喷妥钠影响谷氨酸释放的作用。结果 硫喷妥钠30、100、300μmol/L可明显抑制谷氨酸的自发释放(P<O.01)及KCl诱发的谷氨酸释放(P均<0.01),THS10、THS30、THS100三组之间差异有显著性(P<0.01),但THS100与THS300两组之间差异无显著性(P>0.05)。0.1mmol/L荷包牡丹碱本身对突触体自发释放和KCl诱发释放谷氨酸无明显影响,但硫喷妥钠各浓度组中加入荷包牡丹碱后,谷氨酸释放水平与C组比较差异无显著性(P>0.05)。结论 硫喷妥钠可浓?
Objective To investigate the effect of thiopental sodium (TPS) on spontaneous and KCl-
evoked glutamate release from prefrontal cortical synaptosomes in rats and the effect of bicuculline on this effect of
TPS.Methods SD rats of both sexes (200-250 g) were decapitated and brains were removed. The prefrontal
cortex was dissected and added to ice-cold sucrose solution and homogenized. The homogenate was centrifuged at
1000 g at 0℃-4℃ for 5 min. The supernatant was again centrifuged at 12 000 g for 20 min. The sediment was
crude synaptosomes, which was added to artificial cerebro-spinal fluid (ACSF). The crude synaptosomes were
divided into 5 groups (n = 8): control group and 4 TPS groups. In control group no TPS was added while in TPS
groups different concentrations of TPS was added and the final concentration of TPS was 10, 30, 100, 300μmol·
L^(-1) respectively. The synaptosomes were then placed with or without KCl in water bath at 37℃ for 15 min. The
spontaneous or KCl-evoked glutamate release was measured using high-performance liquid chromatograph (HPLC).
In another set of experiment bicuculline 0. 1 mmol·L^(-1) was added to ACSF in each group before 15 min water bath
to see if it could antogonize the effect of TPS on glutamate release. Results TPS 30, 100 and 300 μmol·L^(-1)
could significantly inhibit the spontaneous or KCl-evoked glutamate release compared with control group (P<
0.01 ). There was significant difference in glutamate release between TPS 30 and TPS 100 groups (P<0. 01 ) but
no significant difference between TPS 100 and 300 groups (P>0.05). Bicuculline 0. 1 mmol·L^(-1) had no effect on
the glutamate release in control group but could antagonize the inhibitory effect of TPS on glutamate release. After
addition of bicucculline the glutamate released in control group was not significantly different from that in the TPS
groups.Conclusion TPS sodium can inhibit the spontaneous or KCl-evoked glutamate release from prefrontal
cortical synaptosomes in a concentration-dependent manner. The inhibitory effect is mediated by GABA_A receptors.
出处
《中华麻醉学杂志》
CAS
CSCD
北大核心
2004年第5期361-364,共4页
Chinese Journal of Anesthesiology
基金
国家自然科学基金(39970715)
江苏省自然科学基金(BK 2001143)
