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Regulation of sleep-wake timing: Circadian rhythms and bistability of sleep-wake states.

機(jī)譯：睡眠-覺醒時(shí)間的調(diào)節(jié)：晝夜節(jié)律和睡眠-覺醒狀態(tài)的雙穩(wěn)態(tài)。

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Sleep is strongly modulated by circadian, homeostatic, and other influences, but little is known about how these factors influence sleep timing. This thesis examined several aspects of sleep timing by studying pathways linked with the ventrolateral preoptic nucleus (VLPO), which has been recently found to promote sleep by inhibiting many of the brain's wake-active monoaminergic arousal systems. Because little was known about afferents to the VLPO, our first aim broadly surveyed afferents to the VLPO using anatomic tracers. Results showed heavy inputs from widespread cortical, hypothalamic, limbic, and brainstem regions. VLPO neurons also received heavy inputs from their own monoaminergic targets, suggesting strong reciprocal connections between sleep- and wake-active systems. Our second aim examined pathways regulating the circadian rhythm of sleep. VLPO neurons receive only sparse inputs from the suprachiasmatic nucleus (SCN), the brain's circadian pacemaker, but we identified a major input from the dorsomedial hypothalamic nucleus (DMH), which receives inputs from the SCN. We found that cell-specific ibotenic acid lesions of the DMH reduced the day-night variation of sleep-wake behavior by 78–89%, with similar reductions of feeding, locomotor activity, and serum corticosteroid rhythms. We also found that the DMH may influence sleep via a mainly GABAergic projection to the VLPO, and a mainly glutamatergic projection to the wake-promoting lateral hypothalamic area, including orexin neurons. Our thud aim examined a neural network model of the reciprocal interactions between sleep- and wake-promoting neurons. Simulations of this circuit exhibited bistable behaviors similar to those observed experimentally, and correctly predicted that lesions of sleep- or wake-promoting neurons would increase the frequency of sleep-wake transitions. Our model also predicted the mathematical distribution of transient arousals during sleep, which have not been accounted for by previous sleep models. Overall, the circadian and stability mechanisms identified in this thesis have implications for understanding the sleep disorder narcolepsy, in which disruptions are seen in both the circadian timing and stability of sleep-wake states.
機(jī)譯：睡眠受到晝夜節(jié)律，體內(nèi)平衡和其他因素的強(qiáng)烈影響，但是對于這些因素如何影響睡眠時(shí)間知之甚少。本論文通過研究與腹外側(cè)視前核（VLPO）相關(guān)的通路，研究了睡眠時(shí)間的幾個(gè)方面，最近發(fā)現(xiàn)該通路通過抑制大腦的許多喚醒活躍的單胺能覺醒系統(tǒng)來促進(jìn)睡眠。由于對VLPO傳入的了解甚少，因此我們的第一個(gè)目標(biāo)是使用解剖示蹤劑廣泛調(diào)查VLPO傳入。結(jié)果表明，來自廣泛的皮質(zhì)，下丘腦，邊緣和腦干區(qū)域的投入很大。 VLPO神經(jīng)元還從其自身的單胺能靶標(biāo)獲得了大量投入，這表明睡眠和喚醒活動系統(tǒng)之間存在強(qiáng)大的相互聯(lián)系。我們的第二個(gè)目標(biāo)檢查了調(diào)節(jié)睡眠晝夜節(jié)律的途徑。 VLPO神經(jīng)元僅從大腦晝夜節(jié)律性起搏器上視神經(jīng)上核（SCN）接收稀疏輸入，但我們從背部丘腦下丘腦核（DMH）識別出主要輸入，DMH從SCN接收輸入。我們發(fā)現(xiàn)，DMH的特定于細(xì)胞的ibotenic酸損害使夜間睡眠覺醒行為的晝夜變化減少了78–89％，同時(shí)進(jìn)食，運(yùn)動能力和血清皮質(zhì)類固醇節(jié)律也有所降低。我們還發(fā)現(xiàn)DMH可能通過對GPO的主要GABA能投射以及對促覺性下丘腦外側(cè)區(qū)域（包括食欲素神經(jīng)元）的主要谷氨酸能投射影響睡眠。我們的目標(biāo)是研究促進(jìn)睡眠和喚醒的神經(jīng)元之間相互相互作用的神經(jīng)網(wǎng)絡(luò)模型。該電路的仿真顯示出與實(shí)驗(yàn)觀察到的相似的雙穩(wěn)態(tài)行為，并且正確地預(yù)測了促進(jìn)睡眠或喚醒的神經(jīng)元的損害會增加睡眠-喚醒轉(zhuǎn)變的頻率。我們的模型還預(yù)測了睡眠期間短暫性喚醒的數(shù)學(xué)分布，以前的睡眠模型并未對此進(jìn)行解釋。總體而言，本文確定的晝夜節(jié)律和穩(wěn)定機(jī)制對于理解睡眠障礙性發(fā)作性睡病具有重要意義，其中在晝夜節(jié)律的定時(shí)和睡眠覺醒狀態(tài)的穩(wěn)定中均可見到破壞。

著錄項(xiàng)

  • 作者

    Chou, Thomas Clayton.;

  • 作者單位

    Harvard University.;

  • 授予單位 Harvard University.;
  • 學(xué)科 Biology Neuroscience.
  • 學(xué)位 Ph.D.
  • 年度 2003
  • 頁碼 133 p.
  • 總頁數(shù) 133
  • 原文格式 PDF
  • 正文語種 eng
  • 中圖分類 神經(jīng)科學(xué);
  • 關(guān)鍵詞

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