An opportunistic theory of cellular and systems consolidation.
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TLDR
This Opinion hypothesizes that the consolidation of hippocampal-dependent memories might not depend on SWS per se, and suggests that the brain opportunistically consolidates previously encoded memories whenever the hippocampus is not otherwise occupied by the task of encoding new memories.About:
This article is published in Trends in Neurosciences.The article was published on 2011-10-01 and is currently open access. It has received 209 citations till now. The article focuses on the topics: Memory consolidation.read more
Citations
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About sleep's role in memory
Bjoern Rasch,Jan Born,Jan Born +2 more
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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Sleep and the Price of Plasticity: From Synaptic and Cellular Homeostasis to Memory Consolidation and Integration
Giulio Tononi,Chiara Cirelli +1 more
TL;DR: This Perspective considers the rationale and evidence for the synaptic homeostasis hypothesis (SHY), and points to open issues related to sleep and plasticity.
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Sleep-dependent memory triage: evolving generalization through selective processing
TL;DR: It is suggested that 'memory triage' lies at the heart of a sleep-dependent memory processing system that selects new information, in a discriminatory manner, and assimilates it into the brain's vast armamentarium of evolving knowledge, helping guide each organism through its own, unique life.
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Sleep, cognition, and normal aging: integrating a half century of multidisciplinary research.
TL;DR: The literature is interpreted as suggesting that maintaining good sleep quality, at least in young adulthood and middle age, promotes better cognitive functioning and serves to protect against age-related cognitive declines.
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Sleep Spindles: Mechanisms and Functions.
TL;DR: Their fine spatiotemporal organization reflects NREMS as a physiological state coordinated over brain and body and may indicate, if not anticipate and ultimately differentiate, pathologies in sleep and neurodevelopmental, -degenerative and -psychiatric conditions.
References
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A synaptic model of memory: long-term potentiation in the hippocampus
TL;DR: The best understood form of long-term potentiation is induced by the activation of the N-methyl-d-aspartate receptor complex, which allows electrical events at the postsynaptic membrane to be transduced into chemical signals which, in turn, are thought to activate both pre- and post Synaptic mechanisms to generate a persistent increase in synaptic strength.
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Why there are complementary learning systems in the hippocampus and neocortex: insights from the successes and failures of connectionist models of learning and memory.
TL;DR: The account presented here suggests that memories are first stored via synaptic changes in the hippocampal system, that these changes support reinstatement of recent memories in the neocortex, that neocortical synapses change a little on each reinstatement, and that remote memory is based on accumulated neocorticals changes.
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The memory function of sleep
Susanne Diekelmann,Jan Born +1 more
TL;DR: Sleep has been identified as a state that optimizes the consolidation of newly acquired information in memory, depending on the specific conditions of learning and the timing of sleep, through specific patterns of neuromodulatory activity and electric field potential oscillations.
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Reactivation of hippocampal ensemble memories during sleep.
TL;DR: In this paper, large ensembles of hippocampal "place cells" were recorded from three rats during spatial behavioral tasks and in slow-wave sleep preceding and following these behaviors, showing an increased tendency to fire together during subsequent sleep, in comparison to sleep episodes preceding the behavioral tasks.
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Fear memories require protein synthesis in the amygdala for reconsolidation after retrieval
TL;DR: It is shown that consolidated fear memories, when reactivated during retrieval, return to a labile state in which infusion of anisomycin shortly after memory reactivation produces amnesia on later tests, regardless of whether reactivation was performed 1 or 14 days after conditioning.