论文部分内容阅读
目的观察氯胺酮对缺氧复氧诱导胎鼠大脑皮层神经细胞谷氨酸释放的影响。方法胎龄16～18d Wistar大鼠的大脑皮层神经细胞,行原代培养,培养的神经细胞随机分为3组,对照组不进行缺氧处理(n=6),缺氧复氧组行缺氧5h复氧(n=6)及氯胺酮组。氯胺酮组随机分为K_1、K_(20)、K_(100)亚组(n=6),均行缺氧5h复氧,K_1、K_(20)、K_(100)组于缺氧前即刻分别予以氯胺酮1、20、100μmol/L终浓度处理。各组于复氧24h时采用高效液相色谱法测定培养液谷氨酸浓度。结果缺氧复氧可导致谷氨酸浓度升高；20、100μmol/L氯胺酮可抑制神经细胞谷氨酸释放,且浓度越高,抑制程度越大。结论氯胺酮可抑制缺氧复氧诱导的胎鼠大脑皮层神经细胞谷氨酸的释放,呈剂量依赖性。
Objective To investigate the effects of ketamine on glutamate release in cultured rat cerebral cortical neurons induced by anoxia / reoxygenation. Methods Cortical neurons of Wistar rats with gestational age of 16-18 days were randomly divided into three groups (n = 6), hypoxia-reoxygenation group Oxygen 5h reoxygenation (n = 6) and ketamine group. Ketamine groups were randomly divided into K_1, K_ (20) and K_ (100) subgroups (n = 6), and hypoxia for 5 hours followed by hypoxia, K_1, K_ (20) and K_ (100) Ketamine 1,20,100μmol / L final concentration of treatment. The levels of glutamic acid in culture medium were determined by high performance liquid chromatography at 24 h after reoxygenation. Results Hypoxia and reoxygenation led to the increase of glutamate concentration. Ketamine at 20 and 100 μmol / L inhibited the glutamate release from neurons, and the higher the concentration, the greater the inhibition. Conclusion Ketamine can inhibit the release of glutamate in neurons exposed to hypoxia-reoxygenation in a dose-dependent manner.