Feng X, Zong Y, Zhang G
Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou 221002.
Yao Xue Xue Bao. 1998 Aug;33(8):561-5.
The relation between Ca2+/CaM PK II activity and excitatoxicity was studied in an in vitro model of rat hippocampal slices. The slices were exposed to 50-200 mumol.L-1 glutamate or 25-100 mumol.L-1 NMDA and glucose-free Krebs buffer for 30 min after being recovered to normal conditions by 2 hours of incubation with standard Krebs buffer. The results showed that inhibition of Ca2+/CaM PK II activity in rat hippocampal slices was induced by exogenous EAA (glutamate or NMDA), and Ca2+/CaM PK II activity values decreased to 50.1% and 44.7% of control at 200 mumol.L-1 glutamate and 100 mumol.L-1 NMDA, respectively; MK801, but not DNQX, antagonized EAA-induced inhibition of Ca2+/CaM PK II activity. When the slices were pretreated with MK801 prior to exposure to 200 mumol.L-1 glutamate or 100 mumol.L-1 NMDA, the Ca2+/Cam PK II activity values were 91.5% and 96.7%, respectively. The changes of extracellular Ca2+ or Mg2+ concentration influenced Ca2+/CaM PK II activity of the slices exposed to exogenous glutamate; Ca2+/CaM PK II activity values in the presence of extracellular Ca2+ was lower than that in the absence of extracellular Ca2+, and it changed from 50.1% of control (presence of Ca2+) to 64% of control (absence of Ca2+) at 200 mumol.L-1 glutamate, but Ca2+/CaM PK II activity values in the presence of extracellular Mg2+ was higher than that in the absence of extracellular Mg2+, and it changed from 50.1% of control(presence of Mg2+) to 36.6% of control (absence of Mg2+) at 200 mumol.L-1 glutamate. The results suggest that NMDA receptor may be involved in excitotoxicity-induced inhibition of Ca2+/CaM PK II activity.
在大鼠海马切片的体外模型中研究了Ca2+/钙调蛋白依赖性蛋白激酶II（Ca2+/CaM PK II）活性与兴奋毒性之间的关系。切片在标准 Krebs 缓冲液中孵育2小时恢复到正常条件后，暴露于50 - 200 μmol·L-1谷氨酸或25 - 100 μmol·L-1 N-甲基-D-天冬氨酸（NMDA）以及无糖的 Krebs 缓冲液中30分钟。结果表明，外源性兴奋性氨基酸（EAA，谷氨酸或NMDA）可诱导大鼠海马切片中Ca2+/CaM PK II活性受到抑制，在200 μmol·L-1谷氨酸和100 μmol·L-1 NMDA作用下，Ca2+/CaM PK II活性值分别降至对照值的50.1%和44.7%；MK801可拮抗EAA诱导的Ca2+/CaM PK II活性抑制，但6,7-二硝基喹喔啉-2,3-二酮（DNQX）无此作用。当切片在暴露于200 μmol·L-1谷氨酸或100 μmol·L-1 NMDA之前用MK801预处理时，Ca2+/钙调蛋白（CaM）PK II活性值分别为91.5%和96.7%。细胞外Ca2+或Mg2+浓度的变化影响暴露于外源性谷氨酸的切片的Ca2+/CaM PK II活性；存在细胞外Ca2+时Ca2+/CaM PK II活性值低于不存在细胞外Ca2+时，在200 μmol·L-1谷氨酸作用下，其从对照值的50.1%（存在Ca2+）变为对照值的64%（不存在Ca2+），但存在细胞外Mg2+时Ca2+/CaM PK II活性值高于不存在细胞外Mg2+时，在200 μmol·L-1谷氨酸作用下，其从对照值的50.1%（存在Mg2+）变为对照值的36.6%（不存在Mg2+）。结果提示NMDA受体可能参与兴奋毒性诱导的Ca2+/CaM PK II活性抑制。
