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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Slow-wave sleep, acetylcholine, and memory consolidation
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Slow-wave sleep, acetylcholine, and memory consolidation

机译：慢波睡眠，乙酰胆碱和记忆巩固

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There has been a long history of experimentation and conjecture about a potentially critical role in memory consolidation for brain processes unique to sleep (1-3). A role for sleep in memory consolidation is consistent with the fact that new memory traces are not instantly fixed but rather remain susceptible to neuro-modulatory influences for several hours after acquisition and require protein synthesis to become stable long-term memories (4). And while it has been clearly demonstrated that sleep deprivation can impair later memory for recently acquired declarative and procedural memory, the precise mechanisms by which sleep may aid or mediate memory storage processes are not known (3, 5). Activation of the cholin-ergic system has been demonstrated to enhance attention, learning, and memory consolidation and to facilitate plasticity after physiological manipulations and during development (6-8). Acetylcholine levels are high during waking and rapid eye movement (REM; also known as paradoxical) sleep (9). These observations seem consistent with the possibility that REM sleep may play an important role in facilitating synaptic plasticity of recently acquired memory traces. However, the great similarities between the waking and REM sleep states beg the question: What about REM sleep relative to waking is privileged for memory consolidation? Explicitly, REM sleep episodes follow deep slow-wave sleep (SWS) episodes. New findings by Gais and Born (10) presented in this issue of PNAS provide compelling evidence in human subjects that SWS and the accompanying low levels of acetylcholine during SWS may mediate a critical memory consolidation process. These findings support two-stage models of memory consolidation, as will be discussed below.
机译：关于睡眠独特的大脑过程在记忆巩固中潜在关键作用的实验和推测已有很长的历史（1-3）。睡眠在记忆巩固中的作用与以下事实相符：新的记忆痕迹并不能立即固定，而是在获取后数小时内仍会受到神经调节的影响，并需要蛋白质合成才能成为稳定的长期记忆（4）。尽管已经清楚地表明睡眠剥夺会损害后来获得的声明性和程序性记忆的后期记忆，但尚不清楚睡眠有助于或介导记忆存储过程的确切机制（3、5）。已证明胆碱能系统的激活可增强注意力，学习和记忆巩固，并在生理学操纵后和发育过程中促进可塑性（6-8）。醒来和快速眼动（REM；也称为自相矛盾）睡眠期间，乙酰胆碱水平很高（9）。这些观察似乎与REM睡眠在促进最近获得的记忆痕迹的突触可塑性中起重要作用的可能性一致。但是，唤醒和REM睡眠状态之间的巨大相似性提出了一个问题：相对于唤醒而言，REM睡眠相对于内存整合有特权吗？明确地说，REM睡眠发作紧随深慢波睡眠（SWS）发作。 Gais和Born（10）在本期PNAS上发表的新发现为人类受试者提供了令人信服的证据，表明SWS和SWS期间伴随的低水平的乙酰胆碱可能介导了关键的记忆整合过程。这些发现支持两阶段的内存整合模型，如下所述。

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