A quartet neural system model orchestrating sleep and wakefulness mechanisms.
A quartet neural system model orchestrating sleep and wakefulness mechanisms.
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DOI：
10.1152/jn.00575.2005
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发表时间：
2006-04
影响因子：
2.5
通讯作者：
Yuichi Tamakawa;A. Karashima;Y. Koyama;N. Katayama;M. Nakao
中科院分区：
文献类型：
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作者：
Yuichi Tamakawa;A. Karashima;Y. Koyama;N. Katayama;M. Nakao
最近有关睡眠/觉醒相关的视前/下丘脑前部和穹窿周（含食欲素）/下丘脑后部神经元的研究结果进一步推进了调节睡眠和觉醒的神经机制的生理学知识。在本文中，我们提出了一个协调睡眠和觉醒四重神经系统机制的数学模型，该系统由以下部分组成：1）睡眠活跃的视前/下丘脑前神经元（N-R组）； 2) 清醒活跃的下丘脑和脑干神经元在清醒期间表现出最高的放电率，在反常或快速眼动（REM）睡眠期间表现出最低的放电率（WA组）； 3) 脑干神经元在快速眼动睡眠期间表现出最高的放电率（快速眼动组）； 4) 基底前脑、下丘脑和脑干神经元在清醒和快速眼动睡眠期间表现出比非快速眼动 (NREM) 睡眠期间更高的放电率（W-R 组）。 WA 神经元与 REM 和 N-R 神经元具有相互抑制耦合。 W-R 神经元与 WA 和 REM 神经元具有相互兴奋性耦合。 REM 神经元受到 N-R 神经元的单向抑制。此外，N-R神经元被两种类型的睡眠促进物质（SPS）激活，它们在睡眠和觉醒的稳态调节中发挥不同的作用。除了状态转换过程中与睡眠相关的神经元活动外，该模型还很好地再现了大鼠的实际睡眠和觉醒模式。此外，只需操纵几个模型参数即可模拟人类睡眠-觉醒节律：N-R 神经元对 REM 和 WA 神经元的抑制增强，并且 N-R 和 WA 神经元的昼夜节律调节被夸大。我们的模型可以为定量理解调节睡眠和觉醒的机制提供一个新颖的框架。
Physiological knowledge of the neural mechanisms regulating sleep and wakefulness has been advanced by the recent findings concerning sleep/wakefulness-related preoptic/anterior hypothalamic and perifornical (orexin-containing)/posterior hypothalamic neurons. In this paper, we propose a mathematical model of the mechanisms orchestrating a quartet neural system of sleep and wakefulness composed of the following: 1) sleep-active preoptic/anterior hypothalamic neurons (N-R group); 2) wake-active hypothalamic and brain stem neurons exhibiting the highest rate of discharge during wakefulness and the lowest rate of discharge during paradoxical or rapid eye movement (REM) sleep (WA group); 3) brain stem neurons exhibiting the highest rate of discharge during REM sleep (REM group); and 4) basal forebrain, hypothalamic, and brain stem neurons exhibiting a higher rate of discharge during both wakefulness and REM sleep than during nonrapid eye movement (NREM) sleep (W-R group). The WA neurons have mutual inhibitory couplings with the REM and N-R neurons. The W-R neurons have mutual excitatory couplings with the WA and REM neurons. The REM neurons receive unidirectional inhibition from the N-R neurons. In addition, the N-R neurons are activated by two types of sleep-promoting substances (SPS), which play different roles in the homeostatic regulation of sleep and wakefulness. The model well reproduces the actual sleep and wakefulness patterns of rats in addition to the sleep-related neuronal activities across state transitions. In addition, human sleep-wakefulness rhythms can be simulated by manipulating only a few model parameters: inhibitions from the N-R neurons to the REM and WA neurons are enhanced, and circadian regulation of the N-R and WA neurons is exaggerated. Our model could provide a novel framework for the quantitative understanding of the mechanisms regulating sleep and wakefulness.