急性乙醇中毒大鼠学习记忆行为的改变与脑组织NO和nNOS含量变化

目的：通过观察急性乙醇中毒对大鼠学习记忆的影响并测定脑组织中一氧化氮（NO）与神经型一氧化氮合酶（nNOS）含量的变化，探讨乙醇中毒影响学习记忆的分子机制。方法:成年SD大鼠随机分为2组，模型组腹腔1次性注射乙醇2.5 g/kg［用生理盐水配成含20%乙醇(W/V)溶液］制备急性乙醇中毒大鼠模型；对照组注射等容量的生理盐水。Y-型迷宫检测大鼠学习记忆成绩、硝酸还原酶法检测鼠脑海马CA1、新纹状体中NO的含量、免疫组化方法检测鼠脑海马CA1、纹状体、小脑中nNOS的含量。结果:（1）模型组大鼠达到学会标准所需要的训练次数（34.33±13.04）明显大于对照组（27.50±8.79），P<0.05；（2）海马CA1区NO的含量在模型组为23.09±9.60，明显高于对照组（8.46±5.67）（P<0.01）；新纹状体（尾壳核）NO的含量在模型组（19.46±8.25）也明显高于对照组（8.22±4.46），P<0.01；（3）海马CA1区nNOS阳性神经元的数量在模型组为18.22±7.47，明显高于对照组（10.15±4.24）（P<0.05）；新纹状体（尾壳核）nNOS阳性神经元的数量在模型组（11.38±5.00）也明显高于对照组（6.15±3.69），P<0.05。结论:乙醇的神经毒性作用可能与脑组织中nNOS和 NO信号通路有关。

Behavior changes of learning and memory related to the levels of NO and nNOS in brain of rats with acute alcoholism

AIM: In order to investigate the molecular mechanism of alcoholism acting on learning and memory, the dysfunction of learning and memory function was observed and the content of nitric oxide (NO) and neuronal nitric oxide synthase (nNOS) were determined in rats with acute alcoholism. METHODS: The mature male Sprague-Dawley rats were randomly divided into two groups. The experimental group animals were intraperitoneally administered with ethanol. The control group animals were injected with saline in the same way. The tests of learning and memory were performed at Y-maze after 6 h. Then brains were removed and the content of NO in brain tissue and nNOS expression in hippocampus CA1, corpus striatum were determined, respectively. RESULTS: (1) The training times to reach qualifying standards of Y-maze in experimental group (34.33±13.04) were higher than those in control group (27.50±8.79, P<0.05). (2) The content of NO in experimental group (23.09±9.60) in hippocampus CA1 was significantly increased (P<0.01) compared with that in control group (8.46±5.67). The content of NO in experimental group (19.46±8.25) in corpus striatum was also higher than that in control group (8.22±4.46, P<0.01). (3) The levels of nNOS expression in experimental group (34.33±13.04) in hippocampus CA1 increased significantly (P<0.05) compared with that in control group (27.50±8.79). nNOS positive neurons in experimental group (18.22±7.47) in corpus striatum were also higher than those in control group (10.15±4.24, P<0.05). CONCLUSION: These findings suggest that the mechanism of ethanol neurotoxicity may be partly involved in the signal pathway of NOS and NO in the brain.