氯胺酮对谷氨酸损伤PC12细胞株多巴胺释放的影响  

Effect of Ketamine Administration on Dopamine Release in Glutamate-Induced Injury in PC12 Cells

作　　者：江伟[1] 王莉[1] 金正均[2] 杭燕南[3] 

机构地区：[1]上海交通大学第六人民医院麻醉科,上海200233 [2]上海第二医科大学基础医学院药理学教研室 [3]上海第二医科大学仁济医院麻醉科

出　　处：《上海第二医科大学学报》2005年第10期1034-1036,共3页Acta Universitatis Medicinalis Secondae Shanghai

摘　　要：目的观察氯胺酮持续存在对谷氨酸损伤前、后的神经元样PC12细胞株释放多巴胺的影响。方法制备谷氨酸损伤前、后的神经元样PC12细胞株模型,采用HPLC技术检测加氯胺酮前、后细胞释放的多巴胺的变化。结果氯胺酮无论是单独与细胞孵育,或者与谷氨酸共同处理,均能够抑制细胞释放多巴胺,并呈剂量依赖性。结论氯胺酮持续存在对PC12细胞多巴胺的释放产生抑制作用。Objective To investigate the effect of continuous ketamine administration on the release of dopamine in glutamate-induced injury in PC12 cells. Methods Using high-performance liquid chromatography technique, the effect of intravenous anesthetic ketamine on the release of dopamine was examined before or after exposure to glutamate in neuronal PC12 cells. Results Attenuation release of dopamine was observed in PC12 cells after being exposed continuously to ketamine. It was in a dose-dependent fashion with ketamine. Conclusion It seems from our results to show that continuous exposure to ketamine reduces the dynamics of dopaminergic transmission in neuronal PC12 cells.

关 键 词：N-甲基-D-天冬氨酸受体拮抗剂 氯胺酮 多巴胺 神经毒性 高效液相色谱法 

分 类 号：R96[医药卫生—药理学]