摘要
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。
AIM To investigate the effects of nitric oxide (NO) in nucleus amygdala on sleep and wakefulness (W). METHODS Polysomnography (PSG) and nucleus amygdala microinjection. RESULTS nitric oxide synthase (NOS) inhibitor N nitro L arginine ( L NNA) increased slow wave sleep (SWS) and decreased W, but sodium nitroferricyanide (SNP), a NO donor, not only decreased W but also abolished the sleeppromoting effect of L NNA. L arginine ( L Arg), a precusor of NO, had no direct effect on sleep and W, but blocked the effect of L NNA. Cyclic guanosine monophosphate (cGMP) decreased SWS and increased W, but methylene blue (MB), a guanosine inhibitor, increased SWS and decreased W, and antagonized the W promoting effect of SNP. No significant change of paradoxical sleep (PS) was found in any group. CONCULUSION Nucleus amygdala play an important role in regulating sleep and wakefulness, and NO in nucleus amygdala has W promoting and SWS inhibiting effects mediated by activation of guanylate cyclase and increase of cGMP concentration.
出处
《中国药理学通报》
CAS
CSCD
北大核心
1999年第3期246-248,共3页
Chinese Pharmacological Bulletin
关键词
一氧化氮
环磷酸鸟苷
睡眠
杏仁核
nitric oxide (NO)
cyclic guanosine monophosphate (cGMP)
sleep
nucleus amygdala
