Erasing Synapses in Sleep: Is It Time to Be SHY?

Frank, Marcos G.

doi:10.1155/2012/264378

Cited by 101 publications

(92 citation statements)

References 171 publications

(269 reference statements)

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“…If there is indeed proportional synaptic renormalization that takes place during sleep (most likely involving strengthening as well as downscaling of synapses [95, 96]), then it is probably to counterbalance the necessarily non-proportional synaptic changes across the brain that result from selective attention during wakefulness. Sleep and attention may therefore share a deeper relationship than previously thought, using similar suppression mechanisms to ignore the outside world while simultaneously influencing each other by regulating synaptic plasticity in a complementary way.…”

Section: Discussionmentioning

confidence: 99%

The Yin and Yang of Sleep and Attention

Kirszenblat

Swinderen

2015

Trends in Neurosciences

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Sleep is not a single state, but a complex set of brain processes that supports a number of physiological needs. Sleep deprivation is known to affect attention in many animals, suggesting that a key function of sleep is to regulate attention. Conversely, tasks that require more attention drive sleep need and sleep intensity. Attention involves the ability to filter incoming stimuli based on their relative salience, and this is likely to require coordinated synaptic activity across the brain. This capacity may have only become possible with the evolution of related neural mechanisms that support two key sleep functions: stimulus suppression and synaptic plasticity. We argue here that sleep and attention may have co-evolved as brain states that regulate each other.

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Section: Discussionmentioning

confidence: 99%

The Yin and Yang of Sleep and Attention

Kirszenblat

Swinderen

2015

Trends in Neurosciences

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“…it is thus most improbable that sleep need -to the extent this is determined by learning -is determined solely by Hebbian LTP (or any other single form of synaptic plasticity)" (p. 4 in Ref. 410). Also, molecular markers of synaptic potentiation like arc, BDNF or Calmodulin-dependent-kinase (CaMK) IV are involved in both the potentiation and depression of synaptic strength or other forms of non-Hebbian scaling (1026,1067), questioning that the relative increase and decrease of these markers across sleep and wakefulness, respectively, is actually related to one specific form of synaptic plasticity.…”

Section: Critical Issuesmentioning

confidence: 99%

About Sleep's Role in Memory

Rasch

Born

2013

Physiological Reviews

2,229

2,026

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Over more than a century of research has established the fact that sleep benefits the retention of memory. In this review we aim to comprehensively cover the field of "sleep and memory" research by providing a historical perspective on concepts and a discussion of more recent key findings. Whereas initial theories posed a passive role for sleep enhancing memories by protecting them from interfering stimuli, current theories highlight an active role for sleep in which memories undergo a process of system consolidation during sleep. Whereas older research concentrated on the role of rapid-eye-movement (REM) sleep, recent work has revealed the importance of slow-wave sleep (SWS) for memory consolidation and also enlightened some of the underlying electrophysiological, neurochemical, and genetic mechanisms, as well as developmental aspects in these processes. Specifically, newer findings characterize sleep as a brain state optimizing memory consolidation, in opposition to the waking brain being optimized for encoding of memories. Consolidation originates from reactivation of recently encoded neuronal memory representations, which occur during SWS and transform respective representations for integration into long-term memory. Ensuing REM sleep may stabilize transformed memories. While elaborated with respect to hippocampus-dependent memories, the concept of an active redistribution of memory representations from networks serving as temporary store into long-term stores might hold also for non-hippocampus-dependent memory, and even for nonneuronal, i.e., immunological memories, giving rise to the idea that the offline consolidation of memory during sleep represents a principle of long-term memory formation established in quite different physiological systems.

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“…Further, synaptic downscaling is proposed to occur during SWS, based on the homeostatic regulation observed with these slow oscillations. The hypothesis, which focuses on sleep as a synapticre-balancing mechanism, has received support from a number of integrated experimental findings [32-37], has stimulated much research, and has led to constructive discussion [38-40]. How results consistent with the synaptic homeostasis hypothesis may be reconciled with the cellular results demonstrated here indicative of sleep-dependent maintenance of LTP, remains unknown.…”

Section: The Cellular Impact Of Sleep and Sleep Deprivationmentioning

confidence: 99%

Sleep, Plasticity and Memory from Molecules to Whole-Brain Networks

et al. 2013

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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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Erasing Synapses in Sleep: Is It Time to Be SHY?

Cited by 101 publications

References 171 publications

The Yin and Yang of Sleep and Attention

The Yin and Yang of Sleep and Attention

About Sleep's Role in Memory

Sleep, Plasticity and Memory from Molecules to Whole-Brain Networks

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