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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 calcium ion and protein kinase C (PKC) on the accumulation of extracellular glutamate (GLU) in neurons were observed using in vitro ischemia model of hippocampal slices in rats. The results showed that in hippocampal slices, The extracellular concentration increased 4-fold (from 32 ± 4 to 113 ± 10 pmol / (min.mgPr) .n = 6). N-type calcium channels antagonist daurisoline (DSL) or calcium-free medium can effectively inhibit this increase in concentration (P <0.01). It is suggested that elevated GLU induced by ischemia for 10 minutes is regulated by Ca2 + influx. When brain slices were incubated under ischemic conditions for 30 min, DSL only partially inhibited this accumulation of GLU, whereas calcium-supplemented medium did not. However, this additional accumulation of GLU was completely blocked by PKC inhibitor H-7 and inhibited by PKC PDB agonist; and not affected by the calmodulin inhibitors Calmdazolium and 8-bromo-cAMP. Prompted ischemia 30min, accumulation of extracellular GLU by calcium influx and PKC double regulation.