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首页> 外文期刊>The European Journal of Neuroscience >Inducible and neuronal nitric oxide synthases (NOS) have complementary roles in recovery sleep induction.
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Inducible and neuronal nitric oxide synthases (NOS) have complementary roles in recovery sleep induction.

机译：诱导型和神经型一氧化氮合酶（NOS）在恢复睡眠诱导中具有互补作用。

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Sleep homeostasis is the process by which recovery sleep is generated by prolonged wakefulness. The molecular mechanisms underlying this important phenomenon are poorly understood. We have previously shown that nitric oxide (NO) generation increases in the basal forebrain (BF) during sleep deprivation (SD). Moreover, both NO synthase (NOS) inhibition and a NO scavenger prevented recovery sleep induction, while administration of a NO donor during the spontaneous sleep-wake cycle increased sleep, indicating that NO is necessary and sufficient for the induction of recovery sleep. Next we wanted to know which NOS isoform is involved in the production of recovery sleep. Using in vivo microdialysis we infused specific inhibitors of NOS into the BF of rats during SD, and found that an inhibitor of inducible NOS (iNOS), 1400W, prevented non-rapid eye movement (NREM) recovery, while an inhibitor of neuronal NOS (nNOS), L-N-propyl-arginine, decreased REM recovery but did not affect NREM recovery. Using immunoblot analysis we found that iNOS was not expressed during the spontaneous sleep-wake cycle, but was induced by prolonged wakefulness (increased by 278%). A known iNOS inducer, lipopolysaccharide, evoked an increase in sleep that closely resembled recovery sleep, and its effects were abolished by 1400W. These results suggest that the elevation of NO produced by induction of iNOS in the BF during prolonged wakefulness is a specific mechanism for producing NREM recovery sleep and that the two NOS isoforms have a complementary role in NREM and REM recovery induction.
机译：睡眠稳态是长时间的清醒使睡眠恢复的过程。对这一重要现象的分子机制了解甚少。先前我们已经表明，在睡眠剥夺（SD）期间，基础前脑（BF）中一氧化氮（NO）的产生增加。而且，NO合酶（NOS）的抑制和NO清除剂均阻止了恢复性睡眠的诱导，而在自发性睡眠-觉醒周期期间施用NO供体增加了睡眠，表明NO对于诱导恢复性睡眠是必要的和充分的。接下来，我们想知道哪种NOS亚型与恢复睡眠的产生有关。通过体内微透析，我们在SD期间向大鼠的BF中注入了NOS的特异性抑制剂，发现1400W的诱导型NOS（iNOS）抑制剂阻止了非快速眼动（NREM）的恢复，而神经元NOS的抑制剂（ nNOS），LN-丙基-精氨酸降低了REM的恢复，但不影响NREM的恢复。使用免疫印迹分析，我们发现iNOS在自发的睡眠-觉醒周期中不表达，但由长时间的清醒诱导（增加了278％）。已知的iNOS诱导剂脂多糖引起的睡眠增加与恢复性睡眠非常相似，并且其作用在1400W时被取消。这些结果表明，在长时间的清醒过程中，BF中由iNOS诱导产生的NO升高是产生NREM恢复睡眠的特定机制，并且这两种NOS亚型在NREM和REM恢复诱导中具有互补作用。

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