Cognitive neuroscience of sleep.
Cognitive neuroscience of sleep.
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DOI：
10.1016/b978-0-444-53702-7.00001-4
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发表时间：
2010
影响因子：
--
通讯作者：
Van Dongen, Hans P. A.
中科院分区：
文献类型：
--
作者：
Kerkhof, Gerard A.;Van Dongen, Hans P. A.
关键词：
机制是理解的核心，本章讨论了潜在的大脑机制和认知途径以及睡眠对这些过程的影响，特别是那些服务于学习和记忆的过程。本章从基本神经生理学研究的角度回顾了当前对睡眠/清醒状态与认知之间关系的理解。睡眠机制与学习和记忆过程的神经生理学之间的广泛重叠为睡眠和学习系统之间的功能联系理论奠定了基础。每一种睡眠状态及其伴随的神经生理学变化都与重要的功能性学习和记忆过程的促进有关。对于快速眼动 (REM) 睡眠，诸如 PGO 波、θ 同步、乙酰胆碱增加、单胺水平降低以及神经元内可塑性相关基因转录增加等显着特征，逐渐允许自由发生的双向可塑性（长时程增强 (LTP) 及其逆转、去增强）。因此，快速眼动睡眠提供了一种新的神经环境，在这种环境中，学习和认知所必需的突触重塑可以发生，至少在海马复合体内是这样。在非快速眼动睡眠第二阶段纺锤波期间，去甲肾上腺素能细胞的停止和随后的强烈爆发以及海马和皮质目标的同时重新激活也将增加突触可塑性，从而允许新皮质中的有针对性的双向可塑性。在 delta 非快速眼动睡眠中，与慢波 delta 活动同相的有序神经元再激活事件，以及高蛋白质合成水平，将促进将早期 LTP 转化为持久 LTP 的事件。相反，Delta 睡眠不会激活与 de novo LTP 相关的早期基因。这种非快速眼动睡眠独特的遗传环境与低乙酰胆碱水平相结合，可能会降低皮质回路的强度，这些回路在约 50% 的 delta 重激活事件中激活，而这些事件不会出现在清醒的放电序列中。本章回顾了操纵研究的结果，通常是完全睡眠或快速眼动睡眠剥夺，这些研究有助于强调现象学关联的功能意义。最后，将从更大的角度考虑睡眠神经生理学对学习和记忆的影响，其中特定睡眠状态与增强或减弱的关联被整合到认知的机械模型中。
Mechanism is at the heart of understanding, and this chapter addresses underlying brain mechanisms and pathways of cognition and the impact of sleep on these processes, especially those serving learning and memory. This chapter reviews the current understanding of the relationship between sleep/waking states and cognition from the perspective afforded by basic neurophysiological investigations. The extensive overlap between sleep mechanisms and the neurophysiology of learning and memory processes provide a foundation for theories of a functional link between the sleep and learning systems. Each of the sleep states, with its attendant alterations in neurophysiology, is associated with facilitation of important functional learning and memory processes. For rapid eye movement (REM) sleep, salient features such as PGO waves, theta synchrony, increased acetylcholine, reduced levels of monoamines and, within the neuron, increased transcription of plasticity-related genes, cumulatively allow for freely occurring bidirectional plasticity (long-term potentiation (LTP) and its reversal, depotentiation). Thus, REM sleep provides a novel neural environment in which the synaptic remodeling essential to learning and cognition can occur, at least within the hippocampal complex. During nonREM sleep Stage 2 spindles, the cessation and subsequent strong bursting of noradrenergic cells and coincident reactivation of hippocampal and cortical targets would also increase synaptic plasticity, allowing targeted bidirectional plasticity in the neocortex as well. In delta nonREM sleep, orderly neuronal reactivation events in phase with slow wave delta activity, together with high protein synthesis levels, would facilitate the events that convert early LTP to long lasting LTP. Conversely, delta sleep does not activate immediate early genes associated with de novo LTP. This nonREM sleep-unique genetic environment combined with low acetylcholine levels may serve to reduce the strength of cortical circuits that activate in the ~50% of delta-coincident reactivation events that do not appear in their waking firing sequence. The chapter reviews the results of manipulation studies, typically total sleep or REM sleep deprivation, that serve to underscore the functional significance of the phenomenological associations. Finally, the implications of sleep neurophysiology for learning and memory will be considered from a larger perspective in which the association of specific sleep states with both potentiation or depotentiation is integrated into mechanistic models of cognition.