论文部分内容阅读
目的研究外源性谷氨酸对海马脑片Ｃａ２＋／ＣａＭＰＫⅡ活性的影响及氯胺酮的保护作用，同时研究缺氧对神经元外谷氨酸堆积的影响。方法采用体外培养的大鼠海马脑片研究这些作用。结果（１）海马脑片在体外缺氧３０ｍｉｎ，谷氨酸在胞外的堆积增加２倍多；（２）单纯过量外源性谷氨酸能引起酶活性显著下降，仅为对照组的２４％，提示脑缺氧时酶活性的抑制与兴奋毒性有关；（３）氯胺酮对单纯外源性谷氨酸所诱导的酶活性抑制有明显的拮抗作用，说明脑缺氧引起酶活性下降与ＮＭＤＡ受体介导有关。结论脑缺氧时该酶活性的抑制与下列通路有关：谷氨酸→ＮＭＤＡ受体→Ｃａ２＋→Ｃａ２＋靶酶。
Objective To study the effect of exogenous glutamate on the activity of Ca2 + / CaMPKⅡ in hippocampal slices and the protective effect of ketamine, and to study the effect of hypoxia on glutamate accumulation in neurons. Methods The rat hippocampal slices cultured in vitro were used to study these effects. Results (1) The hippocampal slices in vitro 30min hypoxia, accumulation of extracellular glutamate increased more than 2 times; (2) Exogenous glutamate alone caused a significant decrease in enzyme activity, only the control group 24 %, Suggesting that the inhibition of enzyme activity in hypoxia was related to excitotoxicity; (3) Ketamine had a significant antagonistic effect on the inhibition of glutamate-induced enzyme activity, indicating that hypoxia-induced hypoxia decreased the activity of NMDA Receptor-mediated. Conclusions The inhibition of the enzyme activity during hypoxia is related to the following pathways: glutamate → NMDA receptor → Ca2 + → Ca2 + target enzyme.