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目的 阐释川楝素的作用机制 ,为了解递质解释的基本过程提供线索。方法 以大鼠大脑皮层匀浆经密度梯度离心分离获得的突触体作为研究标本 ,分别施加 5 0mmol·L- 1KCl,1.5 μmol·L- 1卡西霉素或 7.5mmol·L- 14 氨基吡啶触发谷氨酸 (Glu)释放。通过检测由Glu氧化脱氢反应与NAD+ 生成的NADH荧光变化测定Glu释放量。结果 川楝素浓度、时间依赖地显著抑制由KCl诱发的Glu释放 ,并主要抑制钙依赖性释放 ;由卡西霉素直接提升胞内钙离子浓度而诱发的Glu释放也被川楝素明显抑制。结论川楝素抑制中枢突触Glu释放 ,该效应与其导致的递质释放机制中钙离子敏感性降低有关。
Objective To elucidate the mechanism of toosendanin and provide clues for understanding the basic process of the transmission of mass. Methods The synaptosomes isolated from rat cerebral cortex homogenates by density gradient centrifugation were used as research samples. Fifty mmol·L -1 KCl, 1.5 μmol·L -1 calicheamicin or 7.5 mmol·L -1 aminopyridine Triggered glutamate (Glu) release. The amount of Glu released was measured by measuring the change in NADH fluorescence generated by the oxidative dehydrogenation of Glu and NAD +. Results Toosendanin significantly and significantly inhibited the release of Glu induced by KCl at a concentration-dependent and time-dependent manner, and mainly inhibited the calcium-dependent release. Glu release induced by direct intracellular calcium concentration increase was also significantly inhibited by toosendanin . Conclusion Toosendanin can inhibit the release of glutamate in the central synapse, which is related to the decrease of calcium sensitivity in the mechanism of neurotransmitter release.