钙离子和蛋白激酶C对大鼠缺血海马脑片谷氨酸堆积的影响  

Effects of Ca￣(2+) and Protein Kinase C on Glutamate Accumulation in Rat Hippocampal Slices under Ischemic States

作　　者：卢步峰[1] 鲁友明 黄诒森[1] 

机构地区：[1]镇江医学院生化研究室,海军神经生物学研究中心

出　　处：《生物化学杂志》1995年第1期104-107,共4页

基　　金：江苏省自然科学基金

摘　　要：采用大鼠海马脑片体外缺血模型观察钙离子和蛋白激酶Ｃ（ＰＫＣ）对神经元胞外谷氨酸（ＧＬＵ）堆积的影响，结果显示：海马脑片在体外“缺血”１０ｍｉｎ，ＧＬＵ在胞外的浓度增加４倍（从３２±４升高到１１３±１０ｐｍｏｌ／（ｍｉｎ．ｍｇＰｒ）．ｎ＝６）．Ｎ型钙通道拮抗剂蝙蝠葛苏林碱（ＤＳＬ）或无钙培养液均能有效抑制这种浓度的升高（Ｐ＜０．０１）．提示缺血１０ｍｉｎ引发的ＧＬＵ浓度升高是受Ｃａ２＋内流调控的．当脑片在缺血状况下孵育３０ｍｉｎ，ＤＳＬ只部分抑制这种ＧＬＵ堆积，而无钙培养液则无影响，但这额外的ＧＬＵ堆积可被ＰＫＣ抑制剂Ｈ－７完全阻断，而被ＰＫＣ激动剂ＰＤＢ所加强；且不受钙调蛋白抑制剂Ｃａｌｍｄａｚｏｌｉｕｍ和８－溴－ｃＡＭＰ影响．提示缺血３０ｍｉｎ，胞外ＧＬＵ的堆积受钙内流和ＰＫＣ双重调控。The effects of Ca2+ and protein kinase C (PKC) on glutamate (GLU) accumulation in rat hippocampal shces under in vitro ischemic states has been studied. The results showed that in hippocampal slices, the extracellular concentration of GLU increased four-fold under 10min in vitro ischemic insult (from 32±4 to 113±10 pmol/(min·mg protein).n=6). Since daurisoline,a drug that blocks N-type Ca2+ channels,or Ca2+-free solution potently and effectively lowered this stimulated accumulation (P<0.01),it was predicted that the GLU accumulation was mediated by Ca2+ influx in nerve terminals. When the slices were incubated for 30min under ischemic condition,daurisoline caused only small alteration in the post ischemic accumulation of GLU.However,the extra GLU accumulation was markedly attenuated by H-7.and increased by PDB, whereas 8-bromo-cAMP and calmidazolium was without effect.These results suggested that during a 30min ischemic insult.PKC involved in the GLU accuriulation of supernatant.

关 键 词：钙离子 蛋白激酶 海马脑片 谷氨酸堆积 脑缺血 

分 类 号：R743.310.2[医药卫生—神经病学与精神病学]