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目的研究杏仁核中一氧化氮（ＮＯ）对大鼠睡眠觉醒的影响，并分析其作用机制。方法多导睡眠描记和杏仁核微量注射。结果一氧化氮合酶抑制剂Ｌ硝基精氨酸（ＬＮＮＡ）可增加慢波睡眠（ＳＷＳ）和减少觉醒（Ｗ），而一氧化氮（ＮＯ）供体硝普钠（ＳＮＰ）可增加Ｗ、减少ＳＷＳ，并可对抗ＬＮＮＡ的促睡眠效应；ＮＯ前体Ｌ精氨酸（ＬＡｒｇ）对睡眠觉醒无直接影响，但可对抗ＬＮＮＡ的促睡眠效应。环磷酸鸟苷（ｃＧＭＰ）具有明显的增加Ｗ和减少ＳＷＳ效应，而鸟苷酸环化酶抑制剂亚甲蓝（ＭＢ）增加睡眠、减少觉醒，并可阻断ＳＮＰ的促睡眠效应。结论杏仁核参与睡眠觉醒调节，杏仁核中ＮＯ具有促进Ｗ、抑制ＳＷＳ效应，这一作用是通过激活鸟苷酸环化酶使ｃＧＭＰ增多实现的。
Objective To study the effect of nitric oxide (NO) in amygdala on sleep-wakefulness in rats and its mechanism of action. Methods polysomnography and amygdala microinjection. Results Nitric oxide synthase inhibitor L-NNA increased SWS and decreased awakening, while nitric oxide (NO) donor sodium nitroprusside (SNP) Can increase W, reduce SWS and L-NNA can promote the effect of promoting sleep; NO precursor L arginine (L Arg) has no direct effect on sleep arousal, but can fight L NNA to promote sleep effect. Cyclic guanosine monophosphate (cGMP) significantly increased W and decreased SWS effects, while guanylate cyclase inhibitor methylene blue (MB) increased sleep, decreased arousal, and blocked the effect of SNP on sleep. Conclusion The amygdala participates in sleep-wake regulation. NO in the amygdaloid nucleus promotes W and inhibits SWS. This effect is mediated by the activation of guanylate cyclase to increase cGMP.