Sleep Is for Forgetting

Poe, Gina R.

doi:10.1523/jneurosci.0820-16.2017

Cited by 111 publications

(105 citation statements)

References 110 publications

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“…Sleep has a function in modulating brain plasticity, but its characteristics in relation to the clinical phenotype of PD have not yet been addressed.…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, SWA‐NREM sleep seems to act as a regulator of Hebbian plasticity, preventing saturation of the neuronal network by a sleep‐related synaptic downscaling process . Although the SHY requires further confirmation, the key role of sleep in brain plasticity is well supported by morphological evidence of sleep‐dependent volumetric reduction of synaptic boutons . Furthermore, drug‐induced potentiation of SWA with urethane reduced corticocortical and corticostriatal responses in vivo .…”

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confidence: 97%

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Levodopa‐induced dyskinesia in Parkinson disease: Sleep matters

Amato¹,

Manconi²,

Sarasso

et al. 2018

Annals of Neurology

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Objective: The spectrum of clinical symptom changes during the course of Parkinson disease (PD). Levodopa therapy, while offering remarkable control of classical motor symptoms, causes abnormal involuntary movements as the disease progresses. This levodopa-induced dyskinesia (LID) has been associated with abnormal cortical plasticity. Because slow wave activity (SWA) of nonrapid eye movement (NREM) sleep underlies adjustment of cortical excitability, we sought to elucidate the relationship between this physiological process and LID. Methods: Thirty-six patients at different stages of PD underwent whole-night video polysomnography-high-density electroencephalography (vPSG-hdEEG), preceded by 1 week of actigraphy. To represent the broad spectrum of the disease, patients were divided into 3 groups by disease stage-(1) de novo (n = 9), (2) advanced (n = 13), and (3) dyskinetic (DYS; n = 14)-were compared to an age-matched control group (n = 12). The SWA-NREM content of the vPSG-hdEEG was then temporally divided into 10 equal parts, from T1 to T10, and power and source analyses were performed. T2-T3-T4 were considered early sleep and were compared to T7-T8-T9, representing late sleep. Results: We found that all groups, except the DYS group, manifested a clear-cut SWA decrease between early and late sleep. Interpretation: Our data demonstrate a strong pathophysiological association between sleep and PD. Given that SWA may be a surrogate for synaptic strength, our data suggest that DYS patients do not have adequate synaptic downscaling. Further analysis is needed to determine the effect of drugs that can enhance cortical SWA in LID.

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“…Sleep has a function in modulating brain plasticity, but its characteristics in relation to the clinical phenotype of PD have not yet been addressed.…”

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

Levodopa‐induced dyskinesia in Parkinson disease: Sleep matters

Amato¹,

Manconi²,

Sarasso

et al. 2018

Annals of Neurology

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“…A core question is whether synaptic plasticity and information processing are occurring during just one or both of the two main stages of sleep, NREM and REM. Studies show that both are important for learning and memory, although their relative roles remain a topic of intense debate (54)(55)(56)(57)(58). Evidence suggests that REM may be more associated with local circuit changes reflecting memory consolidation (59) while during NREM global synaptic homeostasis and inter-region memory transfer may dominate (20,60).…”

Section: Theory Of Sleep For Neural Reorganizationmentioning

confidence: 99%

“…Evidence suggests that REM may be more associated with local circuit changes reflecting memory consolidation (59) while during NREM global synaptic homeostasis and inter-region memory transfer may dominate (20,60). Other evidence (58,61,62) suggests that synaptic pruning and reconnection primarily take place during REM sleep, while other results and arguments have posited that NREM sleep is when pruning and reorganizing occur (56).…”

Section: Theory Of Sleep For Neural Reorganizationmentioning

confidence: 99%

Unraveling Why We Sleep: Quantitative Analysis Reveals Abrupt Transition from Neural Reorganization to Repair in Early Development

Cao

Herman

West

et al. 2019

Preprint

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Sleep serves disparate functions, most notably neural repair, metabolite clearance and circuit reorganization, yet the relative importance of these functions remains hotly debated. Here, we create a novel mechanistic framework for understanding and predicting how sleep changes during ontogeny (why babies sleep twice as long as adults) and across phylogeny (why mice sleep roughly five times that of whales). We use this theory to quantitatively distinguish between sleep used for neural reorganization versus repair. We conduct a comprehensive, quantitative analysis of human sleep using total sleep time, cere-bral metabolic rate, brain size, synaptic density, and REM sleep (used here to also refer to Active Sleep in infants and children). Our findings reveal an abrupt transition, between 2 and 3 years of age in humans. Specifically, our results show that differences in sleep across phylogeny and during late ontogeny (after 2 or 3 years in humans) are primarily due to sleep functioning for repair or clearance, while changes in sleep during early ontogeny (before 2 -3 years in humans) primarily support neural reorganization and learning. Moreover, our analysis shows that neuroplastic reorganization occurs primarily in REM sleep but not in NREM. In accordance with the developmental role of neuroplasticity, the percent of time spent in REM sleep is independent of brain size across species but decreases dramatically as brain size grows through development. Furthermore, the ratio of NREM sleep time to awake time emerges as a new invariant across development. This developmental transition and fundamental shift across ontogeny and phylogeny suggests a complex interplay between developmental and evolutionary constraints on sleep.

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“…As recently acquired memories undergo long-term storage [3,4,6,7], memories encoded by the hippocampus (HPC) are stabilized into neocortical regions, where cortico-cortical connections are slowly established and strengthened [8][9][10]. As a consequence, memory corticalization can support successful memory retrieval, can promote reconsolidation, or can prompt forgetting [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Memory corticalization triggered by REM sleep: mechanisms of cellular and systems consolidation

Almeida-Filho

Queiroz

Ribeiro

2018

Cell. Mol. Life Sci.

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Once viewed as a passive physiological state, sleep is a heterogeneous and complex sequence of brain states with essential effects on synaptic plasticity and neuronal functioning. Rapid-eye-movement (REM) sleep has been shown to promote calcium-dependent plasticity in principal neurons of the cerebral cortex, both during memory consolidation in adults and during post-natal development. This article reviews the plasticity mechanisms triggered by REM sleep, with a focus on the emerging role of kinases and immediate-early genes for the progressive corticalization of hippocampus-dependent memories. The body of evidence suggests that memory corticalization triggered by REM sleep is a systemic phenomenon with cellular and molecular causes.

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Sleep Is for Forgetting

Cited by 111 publications

References 110 publications

Levodopa‐induced dyskinesia in Parkinson disease: Sleep matters

Levodopa‐induced dyskinesia in Parkinson disease: Sleep matters

Unraveling Why We Sleep: Quantitative Analysis Reveals Abrupt Transition from Neural Reorganization to Repair in Early Development

Memory corticalization triggered by REM sleep: mechanisms of cellular and systems consolidation

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