摘要
目的了解依托咪酯是否通过抑制突触前神经递质释放而影响中枢突触传递的。方法利用SD大鼠新鲜分离的大脑皮层突触体,以50mmol/L KCl为化学刺激剂去极化。采用高效液相测定法,测定依托咪酯对去极化诱发突触体神经递质谷氨酸和GABA释放的影响。结果不同浓度的依托咪酯(0.4、4和40μmol/L)分别抑制大鼠大脑皮层突触体钙依赖的兴奋性氨基酸谷氨酸(抑制率为对照值的13%,25%和30%)和抑制性氨基酸GABA(抑制率为对照值的7%,16%和37%)的释放。结论依托咪酯抑制突触前神经递质-谷氨酸和GABA的释放,提示依托咪酯在突触前水平可能通过下调突触传递,而使整个大脑皮层处于低水平的兴奋/抑制平衡状态。
Purpose To identify whether etomidate could depress KCl-induced neurotransmitters release from nerve terminals,which underlie central synaptic transmission inhabitation. Methods KCl of 50 mmol/L were used to depolorize the freshly isolated SD rat cerebrocortical synaptosomes. The effects of etomidate on Glutamate and GABA release from synaptosomes were examined with inverse phase high performance liquid chromatographic methods. Results Intravenous anesthetic agent etomidate （0.4,4,40μmol/L） inhibited calcium-dependent excitatory neurotransmitter glutamate（inhibitory ratio was 13 % ,25 % and 30 % compared with control, respectively） and inhibitory neurotransmitter GABA（inhibitory ratio was 7 %, 16 % and 37 % compared with control, respectively） release from rat cerebrocortical synaptosomes. Conclusions Etomidate depressed KCl-induced neurotranmitters-glutamate and GABA-release from rat cerebrocortical synaptosomes, which implied etomidate may produce its presynaptic effects via balancing excitatory/inhibitory neurotransmitters level.
出处
《复旦学报（医学版）》
CAS
CSCD
北大核心
2006年第2期209-212,共4页
Fudan University Journal of Medical Sciences
关键词
依托咪酯
突触传递
突触体
神经递质
etomidate
synaptic transmission
synaptosomes
neurotransmitters
