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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。方法将144只Wistar大鼠随机分组为捕食应激组(n=72)及正常对照组(n=72),在大鼠捕食应激PTSD动物模型基础上,动态检测大鼠海马、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。结果应激大鼠海马NO含量于捕食应激后即刻明显高于对照组犤(2.8±0.8)μmol/g,F=23.112,P=0.000犦,12h达高峰(3.9±1.1)μmol/g,与对照组比较,F=56.616,P=0.000;与同组其他时相比较,F=14.917,P<0.05,24h时仍明显增多犤(2.6±0.7)μmol/g,F=23.094,P=0.000犦;海马nNOS表达亦同步增高(应激后即刻,12及24h,F=14.228,21.772,18.500,P<0.01),而海马总NOS活性仅在应激后12h内增高犤应激后即刻及12hNOS分别为(9.8±2.5)mmol/(s·kg),F=32.812,P=0.000及(10.2±2.7)mmol/(s·kg),F=31.395,P=0.000犦。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。
Objective To investigate the changes of nitric oxide (NO) in post-traumatic stress disorder (PTSD) -like rats and to further reveal the neurobiological mechanism of PTSD. Methods One hundred and forty-four Wistar rats were randomly divided into predator stress group (n = 72) and normal control group (n = 72). Based on the animal model of prey stress-induced PTSD, the dynamic changes of hippocampus and frontal cortex Tissue homogenate NO, nitric oxide synthase (NOS) content and neuronal NOS (nNOS) expression were observed. Results The NO level in the hippocampus of stressed rats was significantly higher than that of the control group (2.8 ± 0.8μmol / g, F = 23.112, P = 0.000犦) and reached the peak at 12h (3.9 ± 1.1μmol / g) Compared with the control group, F = 56.616, P = 0.000; F = 14.917, P <0.05, significantly increased at 24 h (± 2.6 ± 0.7) μmol / g, F = 23.094, P = 0.000 犦; hippocampal nNOS expression also increased simultaneously (immediately after stress, 12 and 24h, F = 14.228,21.772,18.500, P <0.01), while the total hippocampal NOS activity increased only within 12h after stress 犤 immediately after stress And 12hNOS were (9.8 ± 2.5) mmol / (s · kg), F = 32.812, P = 0.000 and 10.2 ± 2.7 mmol / (s · kg), respectively. Conclusion The sustained high expression of nNOS and NO release in hippocampus induced by severe psychological / physiological stress may be significantly increased, which may play an important role in persistent PTSD-like behavioral abnormalities in experimental rats.