论文部分内容阅读
采用大鼠海马脑片体外缺血模型，观察了“缺血”或谷氨酸及氯胺酮对海马脑片Ｃａ￣（２＋）／ＣａＭＰＫⅡ活性的影响，同时观察了缺血对神经元胞外谷氨酸堆积的影响。结果如下：（１）Ｃａ￣（２＋）／ＣａＭＰＫⅡ活性随“缺血”时间的延长而逐渐下降，缺血１０，２０和３０ｍｉｎ，酶活性分别为对照组的６３％，４４％和２９％（１０ｍｉｎ，Ｐ＜０．００２；２０和３０ｍｍ，Ｐ＜０．００１），提示该酶对缺血非常敏感。（２）单纯过量外源性谷氨酸作用３０ｍｉｎ，能引起酶活性显著下降到仅为对照组的２４％，提示脑缺血时酶活性的抑制与兴奋毒性有关。（３）海马脑片在体外缺血３０ｍｉｎ时，谷氨酸在胞外的堆积增加２倍多（从１２８±２０升高到４３１±７４ｎｍｏｌ·ｍｇ￣（－１）ｐｒｏ·ｍｉｎ￣（－１），ｎ＝６）。（４）氯胺酮对“缺血”和单纯外源性谷氨酸所诱导的酶活性抑制均有明显的拮抗作用，但其拮抗作用显著不同，前者可使酶活性恢复至对照的６２％，后者高达９２％。说明脑缺血引起酶活性下降不仅与ＮＭＤＡ受体有关，而且与其它因素有关。
The effects of “ischemia” or glutamate and ketamine on the Ca ~ (2 +) / CaMPKⅡ activity in hippocampal slices were observed using rat hippocampal slice in vitro ischemia model. The effects of ischemia on extracellular glutamate Effect of acid deposition. The results were as follows: (1) The activity of Ca ~ (2 +) / CaMPKⅡ decreased with the time of “ischemia”, and the activities of Ca ~ (2 +) / CaMPKⅡ were 63%, 44% and 29% P <0.002; 20 and 30 mm, P <0.001), suggesting that the enzyme is very sensitive to ischemia. (2) Exogenous glutamate alone 30min, can cause a significant decrease in enzyme activity was only 24% of the control group, suggesting that the inhibition of enzyme activity in cerebral ischemia and excitotoxicity. (3) The accumulation of extracellular glutamate in hippocampal slices increased more than 2 folds (from 128 ± 20 to 431 ± 74 nmol · mg -1 (-1) pro · min -1 ), N = 6). (4) Ketamine had a significant antagonistic effect on the inhibition of the enzyme activity induced by “ischemia” and pure exogenous glutamate, but its antagonism was significantly different. The former restored the enzyme activity to 62% of the control Up to 92%. Cerebral ischemia caused by decreased enzyme activity not only with NMDA receptors, but also with other factors.