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目的研究脑缺血兴奋毒性与Ｃａ２＋／ＣａＭＰＫⅡ的关系。方法采用离体孵育的大鼠海马脑片制备“缺血”模型。采用３２Ｐ标记，滤纸片吸附法测定Ｃａ２＋／ＣａＭＰＫⅡ活性。结果①Ｃａ２＋／ＣａＭＰＫⅡ活性随“缺血”时间延长而降低，“缺血”３０ｍｉｎ可降至正常的１６．４％；②单纯过量外源性谷氨酸作用３０ｍｉｎ可导致Ｃａ２＋／ＣａＭＰＫⅡ活性降低；无胞外Ｃａ２＋时，谷氨酸导致的酶活性抑制程度不如有胞外Ｃａ２＋时显著；③ＭＫ８０１对“缺血”导致的Ｃａ２＋／ＣａＭＰＫⅡ活性抑制有部分拮抗作用，２５μｍｏｌ／ＬＭＫ８０１可使“缺血”３０ｍｉｎ的Ｃａ２＋／ＣａＭＰＫⅡ活性恢复至正常的４３．８％。结论脑缺血导致的Ｃａ２＋／ＣａＭＰＫⅡ活性抑制可被ＭＫ８０１部分拮抗，说明其活性抑制与ＮＭＤＡ受体介导的兴奋性毒性作用有关。
Objective To study the relationship between the excitotoxicity of cerebral ischemia and Ca2 + / CaMPKⅡ. Methods “Ischemia” model was prepared by using rat hippocampal slices incubated in vitro. 32P labeling, filter paper adsorption method for the determination of Ca2 + / CaMPK Ⅱ activity. Results ① The activity of Ca2 + / CaMPKⅡ decreased with the prolongation of “ischemia” time and decreased to normal 16.4% after “ischemia” for 30 minutes. ② Exogenous glutamate increased the activity of Ca2 + / CaMPKⅡ only after 30min exposure to exogenous glutamate Extracellular Ca2 +, glutamate-induced inhibition of enzyme activity was less significant than that of extracellular Ca2 +; ③MK801 had some antagonistic effects on the inhibition of Ca2 + / CaMPKⅡ activity induced by “ischemia”, and 25μmol / LMK801 could make “ischemia” 30 min Of Ca2 + / CaMPKII activity returned to normal 43.8%. Conclusion The inhibition of Ca2 + / CaMPKⅡ activity induced by cerebral ischemia may be partially antagonized by MK801, indicating that the inhibition of its activity is related to the NMDA receptor-mediated excitotoxicity.