Neuropeptide S Counteracts Paradoxical Sleep Deprivation-Induced Anxiety-Like Behavior and Sleep Disturbances.
Neuropeptide S Counteracts Paradoxical Sleep Deprivation-Induced Anxiety-Like Behavior and Sleep Disturbances.
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神经肽 S 可以抵消睡眠不足引起的反常焦虑样行为和睡眠障碍
DOI：
10.3389/fncel.2018.00064
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发表时间：
2018
影响因子：
5.3
通讯作者：
Hou YP
中科院分区：
文献类型：
--
作者：
Xie JF;Shao YF;Wang HL;Wang C;Cui GF;Kong XP;Wang LX;Chen YN;Cong CY;Chen HL;Hou YP
睡眠障碍是焦虑症患者常见的主观抱怨。睡眠不足会增加健康人的一般和特殊焦虑症状。杏仁核是调节焦虑的关键区域，也参与调节情绪对睡眠的影响。神经肽S及其受体是一种新的内源性唤醒和抗焦虑系统，但目前尚不清楚该系统是否参与睡眠剥夺引起的焦虑样行为和睡眠，以及在共病条件下它是如何发挥抗焦虑作用的。用改良多平台法(MMPM)诱导大鼠异相睡眠剥夺(PSD)24 h后，大鼠出现焦虑样行为，睡眠潜伏期延长，异相睡眠(PS)反弹，并伴有脑电(EEG)(4.5~8.5 Hz)跨明暗相脑电活动增加。PSD后PS的增加是由于亮相的发作数增加，暗期的发作数和持续时间增加所致。NPS(1nmol)的中枢作用减弱了PSD诱导的焦虑样行为，并通过增加觉醒和抑制PS和EEG theta活动改变了PSD诱导的睡眠-觉醒障碍。在光相期间给予NPS后PS时间的减少是由于发作次数的减少。此外，给予NPS的PSD大鼠的24小时睡眠时间少于生理盐水对照组。PSD可显著提高杏仁核NPSR基因的表达水平。NPS显著增加杏仁基底外侧核(BLA)、中央杏仁核(CEA)和内侧杏仁核(MeA)内Fos阳性神经元的数量。NPS诱导的大部分Fos-ir神经元也表达NPSR。这些结果表明，杏仁核NPSR的上调可能与PSD诱导的焦虑样行为和睡眠障碍有关，NPS可能通过激活杏仁核中携带NPSR的神经元来对抗PSD诱导的焦虑样行为和睡眠障碍。此外，接受NPS治疗的PSD大鼠的睡眠略有增加，这表明NPS可以起到缓解焦虑的作用，而不会导致随后的睡眠反弹。
Disturbed sleep is a common subjective complaint among individuals with anxiety disorders. Sleep deprivation increases general and specific anxiety symptoms among healthy individuals. The amygdala is critical for regulating anxiety and also involved in mediating the effects of emotions on sleep. Neuropeptide S (NPS) and NPS receptors (NPSR) are reported as a novel endogenous arousal and anxiolytic system, but it is unclear yet whether this system is involved in anxiety-like behavior and sleep caused by sleep deprivation, and how it plays anxiolytic effect underlying the comorbid condition. In the present study, we demonstrate that paradoxical sleep deprivation (PSD) induced by modified multiple platform method (MMPM) for 24 h caused anxiety-like behavior, a prolonged sleep latency and subsequent paradoxical sleep (PS) rebound accompanied by an increase in electroencephalogram (EEG) theta (4.5–8.5 Hz) activities across light and dark phase in rats. The increase of PS after PSD was due to an increase of episode number during light phase and both episode number and duration during dark phase. Central action of NPS (1 nmol) attenuated PSD-induced anxiety-like behavior, and altered PSD-induced sleep-wake disturbances through increasing wakefulness, and suppressing PS and EEG theta activities. The reduction in PS time following NPS administration during light phase was because of a decreased episode number. Furthermore, sleep amount in 24 h in PSD rats given NPS was lesser than that given saline. PSD significantly enhanced NPSR mRNA expression level in the amygdala. NPS remarkably increased the number of Fos-ir neurons in the basolateral amygdala (BLA), the central amygdala (CeA) and medial amygdala (MeA). The majority of Fos-ir neurons induced by NPS also expressed NPSR. These results suggest that NPSR upregulation in the amygdala is presumably related to the PSD-induced anxiety-like behavior and sleep disturbances, and that NPS counteracts PSD-induced anxiety-like behavior and sleep disturbances possibly through activating the neurons bearing NPSR in the amygdala. In addition, the little sleep increase in PSD rats treated with NPS suggests that NPS can function as an anxiolytic without causing a subsequent sleep rebound.
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影响因子：
13.3
作者：
Guerrini, Remo;Salvadori, Severo;Calo, Girolamo
通讯作者：
Calo, Girolamo
影响因子：
3.4
作者：
Lage, Ricardo;Gonzalez, C. Ruth;Lopez, Miguel
通讯作者：
Lopez, Miguel
DOI：
10.1016/j.pnpbp.2012.11.006
发表时间：
2013-03-05
影响因子：
5.6
作者：
Pires, Gabriel N.;Tufik, Sergio;Andersen, Monica L.
通讯作者：
Andersen, Monica L.
影响因子：
3.5
作者：
Ebner, Karl;Rjabokon, Alesja;Pape, Hans-Christian;Singewald, Nicolas
通讯作者：
Singewald, Nicolas
影响因子：
3.7
作者：
Jakubcakova V;Flachskamm C;Landgraf R;Kimura M
通讯作者：
Kimura M