摘要
目的研究Ｃａ２＋和氯胺酮对海马脑片Ｃａ２＋／ＣａＭＰＫⅡ活性的影响。方法采用大鼠海马脑片体外缺氢模型进行实验，结果（１）有钙或无钙培养时，酶活性随缺氧时间的延长均下降，但前者比后者酶活性下降更显著，提示外Ｃａ２＋在神经元缺氧损伤中起重要作用；（２）氯胺酮对缺氧所诱导的酶活性抑制均有明显的拮抗作用，说明脑缺氧引起酶活性下降与ＮＭＤＡ受体介导有关。结论脑缺氧时该酶活性的抑制与下列通路有关：ＮＭＤＡ受体→Ｃａ２＋→Ｃａ２＋靶酶。
Purposes: To examine the effects of Ca2+ and ketamine on Ca2+/CaM PK Ⅱ activity under a condition of hypoxic state in vitro. Methods: The rat hippocampal slice was developed as a model for investigating the above effects. Results: (1) Ca2+/CaM PK Ⅱ activity decreased gradually with increasing hypoxic time in culture medium with or without Ca2+ (1.3 mmol/L), with the decrease much more pronounced in the former case. (2) The inhibition of the enzyme activity induced by either hypoxia could be antagonized markedly by pretreatment with ketamine, showing that the hypoxia-induced inhibition of enzyme activity is mediated by NMDA receptor. Conclution: The brain hypoxia-induced inhibition of the enzyme activity is mediated by the following pathway: NMDA receptor→Ca2+→Ca2+ target enzyme.
出处
《徐州医学院学报》
CAS
1996年第4期334-336,共3页
Acta Academiae Medicinae Xuzhou
基金
国家自然科学基金
