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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Brain serotonin dysfunction accounts for aggression in male mice lacking neuronal nitric oxide synthase
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Brain serotonin dysfunction accounts for aggression in male mice lacking neuronal nitric oxide synthase

机译：脑5-羟色胺功能障碍是缺乏神经元一氧化氮合酶的雄性小鼠攻击性的原因。

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摘要

Genetically engineered mice with targeted disruption of the neu- ronal nitric oxide synthase (nNOS) gene estabIished the inhibitory role of nitric oxide (NO) in male impulsive aggressive behavior. This was later confirmed by using selective nNOS inhibitors in male wild-type mice. The molecular mechanisms accounting for the aggressive behavior caused by the lack of neuronally derived NO is not known. Recent studies suggest that central serotonergic neuronal circuits and particularly 5-HT_1A and 5-HT_1B receptors play. a prominent role in the regulation of aggression. Accordingly. we investigated whether the aggressiveness caused by the lack of nNOS might be because of alterations in serotonergic function. We now demonstrate that the excessive aggressiveness and impul- siveness of nNOS knockout mice is caused by selective decrements in serotonin (5-HT) turnover and deficient 5-HT_1A and 5-HT_1B receptor function in brain regions regulating emotion. These re- sults indicate an important role for NO in normal brain 5-HT function and may have significant implications for the treatment of psychiatric disorders characterized by aggressiveness and impulsivity.
机译：定向破坏神经型一氧化氮合酶（nNOS）基因的基因工程小鼠证实了一氧化氮（NO）在男性冲动攻击行为中的抑制作用。后来通过在雄性野生型小鼠中使用选择性nNOS抑制剂证实了这一点。尚缺乏解释神经元衍生NO缺乏引起的攻击行为的分子机制。最近的研究表明中枢5-羟色胺能神经元回路，尤其是5-HT_1A和5-HT_1B受体起作用。在侵略调节中起着重要作用。因此。我们调查了由nNOS缺乏引起的侵略性是否可能是由于血清素能功能的改变所致。现在我们证明，nNOS基因敲除小鼠的过度攻击和冲动是由血清素（5-HT）转换选择性降低以及调节情绪的大脑区域中的5-HT_1A和5-HT_1B受体功能不足引起的。这些结果表明NO在正常的脑5-HT功能中起重要作用，并且可能对以攻击性和冲动为特征的精神疾病的治疗具有重要意义。

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