摘要
目的 观察依托咪酯(Eto)对海马CA1区兴奋性突触后电位(fEPSP)和长时程抑制(LTD)影响。 方法 利用场电位技术记录大鼠海马脑片CA1区fEPSP。 结果 10 μmol/LEto可显著抑制fEPSP的基础传递,加药后35minfEPSP的幅值为基线值的(71.7±3) % ,与基线相比差异显著(P <0 .0 5 ) ;1μmol/LEto对基础传递无影响,但可易化LTD的诱导。对照组低频后35minfEPSP幅值为基线值的(85±3) % ,而1μmol/LEto组低频后35minfEPSP幅值为基线值的(6 9±2 ) % ,与对照组比较差异有显著性(P <0 .0 5 )。AP 5可以阻断对照组和Eto组LTD的诱导。 结论 Eto呈剂量依赖性地抑制海马CA1区fEPSP ,并且易化LTD的诱导。
Objective To examine the effect of etomidate(Eto) on baseline synaptic transmission and long-term depression(LTD) in the CA1 area of the rat hippocampal slice. Methods Field excitatory post-synaptic potential was recorded. Results 10 μmol/L(Eto) inhibited field excitatory post-synaptic potential(fEPSP) significantly, the fEPSP value was (71.7±3)% of baseline 35min after etomidate administration(P<0.05),compared with baseline. Low dose of etomidate (1 μmol/L) did not affect the basal synaptic transmission, but enhanced prominently the development of LTD. The fEPSP value was (69±2)% of baseline 35 min after LFS in etomidate group(P<0.05),compared with control group[the fEPSP value was (85±3)% of baseline 35 min after LFS]. Conclusion Eto dose-dependently inhibited fEPSP in the CA1 area of rat hippocampus and facilitated LTD induction.
出处
《福建医科大学学报》
2005年第2期133-136,共4页
Journal of Fujian Medical University
基金
福建省自然科学基金资助项目 (C0 3 10 0 12 )