摘要
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 relation between Ca^2+/CaM PK Ⅱ and cerebral ischemia. Methods Studying in an in vitro model of rat hippocampal slice. Results (1)Ca^2+/CaM PK Ⅱ activity decreased with ischemic time increasing, and fell to 16.4% of control at 30 min of ischemia.(2)Treatment with excessive exogenous glutamate for 30 min induced inhibition of Ca^2+/CaM PK Ⅱ activity,and inhibition of the enzyme activity in the absence of extracellular Ca^2+ was less than that in existance of extracellular Ca^2+. (3) 25μmol/L MK801 recovered Ca^2+/CaM PK Ⅱactivity from 16.4% to 43.8% of control at 30 min of ischemia. Conclusions NMDA receptors play an important role in ischemia-induced inhibition of Ca^2+/CaM PK Ⅱ activity.
出处
《徐州医学院学报》
CAS
1997年第6期6-10,共5页
Acta Academiae Medicinae Xuzhou
基金
国家自然科学基金
