捕食应激致大鼠海马NO释放增多及nNOS表达增强

目的：探讨一氧化氮（NO）在创伤后应激障碍（PTSD）样行为异常大鼠的变化规律，以进一步揭示PTSD的神经生物学机制。方法：在大鼠捕食应激PTSD动物模型基础上，动态检测了大鼠海马、额叶皮层组织匀浆NO、一氧化氮合酶（NOS）含量及神经元型NOS（nNOS)表达。结果：PTSD样行为异常大鼠海马NO含量于捕食应激后即刻明显升高，12h达高峰，24h时仍明显增多；海马nNOS表达亦同步增高，而额叶皮层则无明显改变。结论：严重心理生理应激所致海马nNOS持续性高表达与NO释放明显增多，在实验大鼠持续性PTSD样行为异常中可能有重要作用。

Predator stress facilitates NO releasing and neuronal NO synthase expression in hippocampi of rats

Objective To observe the alterations of nitric oxide (NO) and the neuronal NOS (nNOS) in rats with posttraumatic stress disorder (PTSD) like behaviors,and to explore the neurobiological bases in the pathogenesis of PTSD. Methods After establishing the PTSD animal model following non injurious exposure of rats to cat for 10 min, the nitric oxide (NO) and NO synthase (NOS) levels by neurochemistry methods, and the neuronal NOS (nNOS) expression by Western blotting were investigated in hippocampi and frontal cortex of experimental rats. Results The NO levels in hippocampi of experimental rats with PTSD like behaviors were significantly increased immediately, and reached the peak level at 12 h, and still elevated at 24 h after predator stress. The Western analysis demonstrated that the nNOS expression was markedly enhanced synchronously in hippocampi, while no alterations were found in frontal cortex in stress rats. Conclusion The lasting increased nNOS expression and NO releasing in hippocampi following severe psycophysiological stress may play an important role in the long term PTSD like behavior of rats.