亚急性一氧化碳中毒致小鼠迟发性学习记忆障碍机制研究

以亚急性ＣＯ中毒小鼠脑组织Ｃａ＾２＋－Ｍｇ＾２＋ＡＴＰａｓｅ、ＳＯＤ、ＭＡＯ－Ｂ活性，ＬＰＯ含量以及血皮质醇浓度的变化为观察指标，进行亚急性一氧化碳（ＣＯ）中毒致小鼠迟发性学习记忆障碍的机制研究。结果显示，亚急性ＣＯ中毒小鼠脑组织ＳＯＤ、Ｃａ＾２＋－Ｍｇ＾２＋ＡＴＰａｓｅ活性、ＬＰＯ含量以及血皮质醇浓度均无显著改变；而ＭＡＯ－Ｂ活性明显增加，地塞米松对皮质醇分泌的抑制率大为下降。提示，亚急性ＣＯ中

Study on Mechanism of Delayed Learning and Memory Disorders Induced by Subacute Carbon Monoxide Intoxication in Mice

In order to study the pathogenic mechanism of delayed learning and memory damages after subacute CO poisoning,changes in activities of SOD, Ca 2 -Mg 2 ATPase, MAO-B and the content of LPO were measured in brains of mice after CO exposure.The levels of cortisol in serum were also monitored after CO exposure.Results showed that subacute CO poisoning could cause delayed impairments of learning and memory function as well as significant increase of MAO-B activity,however,the activities of SOD,Ca 2 -Mg 2 ATPase and content of LPO had no significant changes.The inhibition effect of Dexamathasone on hypothalamic pituitary adrenal axis was obviously attenuated,although levels of cortisol in serum showed no significant difference between CO exposure group and the control group.These results suggest that changes in monoaminergenic nerve and its transmitter and ineffectiveness in regulation function of hypothalamic pituitary adrenal axis are involved in mechanism of delayed disorders of learning and memory function induced by subacute CO intoxication in mice.