Pei L, Zong Y Y, Zhang L, Sun Y F, Zhang G Y
Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College.
Sheng Li Xue Bao. 1997 Feb;49(1):61-6.
The effects of Ca2+ and ketamine on Ca2+/CaM PK II activity in rat hippocampal slices under in vitro hypoxic states have been studied and the effect of hypoxia on glutamate accumulation was also investigated. The results were as follows: (1) Ca2+/CaM PK II activity decreased gradually with increasing hypoxic time in culture medium with or without 1.3 Ca2- mmol/L, with the former case being much more pronounced. (2) Extracellular accumulation of GLU increased about two-fold after hypoxia for 30 min in vitro. (3) When slices were incubated for 30 min under conditions in excess of exogenous GLU the enzyme activity markedly decreased, a finding suggesting that the inhibition of enzyme activity induced by hypoxia may result from excitotoxicity. (4) The inhibition of the enzyme activity induced by either hypoxia or excess exogenous glutamate alone could be antagonized markedly by pretreatment with ketamine, suggesting that the hypoxia induced inhibition of the enzyme activity is mediated by NMDA receptor.
研究了钙离子（Ca2+）和氯胺酮对体外缺氧状态下大鼠海马切片中Ca2+/钙调蛋白依赖蛋白激酶II（CaM PK II）活性的影响，并研究了缺氧对谷氨酸积累的影响。结果如下：（1）在含有或不含有1.3 mmol/L Ca2+的培养基中，Ca2+/CaM PK II活性随缺氧时间的延长而逐渐降低，在前一种情况下更为明显。（2）体外缺氧30分钟后，细胞外谷氨酸（GLU）积累增加约两倍。（3）当切片在过量外源性GLU条件下孵育30分钟时，酶活性显著降低，这一发现表明缺氧诱导的酶活性抑制可能是由兴奋性毒性引起的。（4）单独缺氧或过量外源性谷氨酸诱导的酶活性抑制可被氯胺酮预处理显著拮抗，这表明缺氧诱导的酶活性抑制是由N-甲基-D-天冬氨酸（NMDA）受体介导的。
