Sleep, plasticity and memory from molecules to whole-brain networks.
Sleep, plasticity and memory from molecules to whole-brain networks.
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从分子到全脑网络的睡眠，可塑性和记忆力。
DOI：
10.1016/j.cub.2013.07.025
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发表时间：
2013-09-09
期刊：
影响因子：
9.2
通讯作者：
Walker, Matthew P.
中科院分区：
文献类型：
--
作者：
Abel, Ted;Havekes, Robbert;Saletin, Jared M.;Walker, Matthew P.
尽管睡眠在整个人类中无处不在，但它的功能仍然难以捉摸。在这篇综述中，我们考虑了一个引人注目的候选人：与记忆加工相关的大脑可塑性。主要集中在啮齿动物和人类的大脑皮层依赖的记忆，我们描述了分子，细胞，网络，全脑和行为的证据建立睡眠的作用，无论是在准备初始的记忆编码，并在随后的离线巩固记忆。睡眠和睡眠剥夺双向改变调节突触强度和控制可塑性相关基因转录和蛋白质翻译的分子信号通路。在细胞水平上，睡眠剥夺损害了诱导突触增强所必需的细胞兴奋性，并加速了突触可塑性的持久形式的衰减。相反，NREM和REM睡眠增强先前诱导的突触增强，尽管在睡眠期间也观察到突触去增强。除了单细胞动力学之外，大规模的细胞集合表达了在随后的睡眠中与先前学习相关的放电模式的协调重放。这种情况发生在海马体、皮质以及海马体和皮质之间，通常与特定的NREM睡眠振荡有关。在全脑水平上，人类在NREM睡眠期间与学习相关的海马（再）激活有些类似。此外，啮齿动物中与重放相关的相同皮层NREM振荡也促进人类海马记忆巩固，并且该过程可以在睡眠期间使用外源性再激活线索进行操纵。在啮齿类动物中发现了一个奇妙的分子现象，编码前的特定NREM睡眠振荡刷新了人类海马的学习能力，而睡眠剥夺反过来损害了随后的海马活动和相关的编码。总之，这些跨描述水平的研究结果表明，睡眠的独特神经生物学对可塑性的分子，细胞和网络机制产生强大的影响，这些机制控制着初始学习和随后的长期记忆巩固。
Despite the ubiquity of sleep across phylogeny, its function remains elusive. In this review, we consider one compelling candidate: brain plasticity associated with memory processing. Focusing largely on hippocampus-dependent memory in rodents and humans, we describe molecular, cellular, network, whole-brain and behavioral evidence establishing a role for sleep both in preparation for initial memory encoding, and in the subsequent offline consolidation ofmemory. Sleep and sleep deprivation bidirectionally alter molecular signaling pathways that regulate synaptic strength and control plasticity-related gene transcription and protein translation. At the cellular level, sleep deprivation impairs cellular excitability necessary for inducing synaptic potentiation and accelerates the decay of long-lasting forms of synaptic plasticity. In contrast, NREM and REM sleep enhance previously induced synaptic potentiation, although synaptic de-potentiation during sleep has also been observed. Beyond single cell dynamics, large-scale cell ensembles express coordinated replay of prior learning-related firing patterns during subsequent sleep. This occurs in the hippocampus, in the cortex, and between the hippocampus and cortex, commonly in association with specific NREM sleep oscillations. At the whole-brain level, somewhat analogous learning-associated hippocampal (re)activation during NREM sleep has been reported in humans. Moreover, the same cortical NREM oscillations associated with replay in rodents also promote human hippocampal memory consolidation, and this process can be manipulated using exogenous reactivation cues during sleep. Mirroring molecular findings in rodents, specific NREM sleep oscillations before encoding refresh human hippocampal learning capacity, while deprivation of sleep conversely impairs subsequent hippocampal activity and associated encoding. Together, these cross-descriptive level findings demonstrate that the unique neurobiology of sleep exert powerful effects on molecular, cellular and network mechanism of plasticity that govern both initial learning and subsequent long-term memory consolidation.
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DOI：
10.1126/science.1202839
发表时间：
2011-06-24
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Bushey D;Tononi G;Cirelli C
通讯作者：
Cirelli C
影响因子：
3.7
作者：
Eschenko, Oxana;Sara, Susan J.
通讯作者：
Sara, Susan J.
影响因子：
5.6
作者：
Dresler, Martin;Kluge, Michael;Steiger, Axel
通讯作者：
Steiger, Axel
影响因子：
3.5
作者：
Alhaider, Ibrahim A.;Aleisa, Abdulaziz M.;Alkadhi, Karim A.
通讯作者：
Alkadhi, Karim A.
影响因子：
5.3
作者：
Andrade, Katia C.;Spoormaker, Victor I.;Czisch, Michael
通讯作者：
Czisch, Michael