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Journal ArticleDOI

The why and how of sleep-dependent synaptic down-selection.

TLDR
Recently, a key molecular mechanism that allows broad synaptic weakening during sleep was identified and other mechanisms still being investigated should eventually explain how sleep can weaken most synapses but afford protection to some, including those directly activated by learning as discussed by the authors.
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This article is published in Seminars in Cell & Developmental Biology.The article was published on 2021-03-09. It has received 18 citations till now. The article focuses on the topics: Biology & Sleep (system call).

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Citations
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Journal ArticleDOI

The two‐process model of sleep regulation: Beginnings and outlook

TL;DR: How animal experiments aimed at exploring the oscillators driving the circadian sleep–wake rhythm led to the recognition of gradients of sleep states within the daily sleep period provided the basis for the first version of the two‐process model.
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Net decrease in spine-surface GluA1-containing AMPA receptors after post-learning sleep in the adult mouse cortex.

TL;DR: In this article, the authors show that sleep leads to an overall net decrease in spine-surface GluA1-containing AMPA receptors and that this is correlated with changes in performance after sleep.
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The inescapable drive to sleep: Overlapping mechanisms of sleep and sedation.

TL;DR: The primal human experience is that a long period without sleep is unsustainable, and it is also detrimental to health and behavior as discussed by the authors, and the powerful and primal urge to sleep after sleep deprivation is int...
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Rapid-acting antidepressants and the circadian clock.

TL;DR: A growing number of epidemiological and experimental studies has established that circadian disruption is strongly associated with psychiatric disorders, including major depressive disorder (MDD), including depression as discussed by the authors, which is becoming increasingly relevant considering that modern lifestyles, social zeitgebers (time cues) and genetic variants contribute to disrupting circadian rhythms that may lead to psychiatric disorders.
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Optimising the energetic cost of the glutamatergic synapse.

TL;DR: In this paper, the authors reviewed how much of the energetic cost of the brain reflects the activity of glutamatergic synapses, considered the relative amount of energy used pre- and postsynaptically, and outlined how evolution has energetically optimised synapse function by adjusting the presynaptic release probability and the postsynaptic number of glutamate receptors.
References
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Journal ArticleDOI

Sleep Drives Metabolite Clearance From the Adult Brain

TL;DR: It is reported that sleep has a critical function in ensuring metabolic homeostasis and convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep, suggesting the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.
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An Energy Budget for Signaling in the Grey Matter of the Brain

TL;DR: The estimates of energy usage predict the use of distributed codes, with ≤15% of neurons simultaneously active, to reduce energy consumption and allow greater computing power from a fixed number of neurons.
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About sleep's role in memory

TL;DR: This review aims 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.
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Neurocognitive Consequences of Sleep Deprivation

TL;DR: Cognitive deficits believed to be a function of the severity of clinical sleep disturbance may be a product of genetic alleles associated with differential cognitive vulnerability to sleep loss.
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Learning Induces Long-Term Potentiation in the Hippocampus

TL;DR: It is found that one-trial inhibitory avoidance learning in rats produced the same changes in hippocampal glutamate receptors as induction of LTP with HFS and caused a spatially restricted increase in the amplitude of evoked synaptic transmission in CA1 in vivo.
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