Memory Takes Time

Kukushkin, Nikolay V.; Carew, Thomas

doi:10.1016/j.neuron.2017.05.029

Cited by 54 publications

(39 citation statements)

References 199 publications

(232 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Bridging the gap between molecular, ultrastructural, and cellular changes on one hand, and behavioral and cognitive effects on the other hand, remains a challenge. Even more so since, it is increasingly appreciated that all these processes, from the turnover of spines (Berry & Nedivi, ) to “memory” (Kukushkin & Carew, ) are highly dynamic, change constantly due to ongoing stimulation, and include multiple overlapping windows that span from minutes to days and weeks. Yet, the past few years have seen significant progress and two general principles have emerged that will be discussed below.…”

Section: Role Of Neuronal Activity In Sleep‐dependent Down‐selection:mentioning

confidence: 99%

Sleep and synaptic down‐selection

Tononi

Cirelli

2019

Eur J of Neuroscience

143

107

View full text Add to dashboard Cite

The synaptic homeostasis hypothesis (SHY) proposes that sleep is an essential process needed by the brain to maintain the total amount of synaptic strength under control. SHY predicts that by the end of a waking day the synaptic connections of many neural circuits undergo a net increase in synaptic strength due to ongoing learning, which is mainly mediated by synaptic potentiation. Stronger synapses require more energy and supplies and are prone to saturation, creating the need for synaptic renormalization. Such renormalization should mainly occur during sleep, when the brain is disconnected from the environment and neural circuits can be broadly reactivated off‐line to undergo a systematic but specific synaptic down‐selection. In short, according to SHY sleep is the price to pay for waking plasticity, to avoid runaway potentiation, decreased signal‐to‐noise ratio, and impaired learning due to saturation. In this review, we briefly discuss the rationale of the hypothesis and recent supportive ultrastructural evidence obtained in our laboratory. We then examine recent studies by other groups showing the causal role of cortical slow waves and hippocampal sharp waves/ripples in sleep‐dependent down‐selection of neural activity and synaptic strength. Finally, we discuss some of the molecular mechanisms that could mediate synaptic weakening during sleep.

show abstract

Section: Role Of Neuronal Activity In Sleep‐dependent Down‐selection:mentioning

confidence: 99%

Sleep and synaptic down‐selection

Tononi

Cirelli

2019

Eur J of Neuroscience

143

107

View full text Add to dashboard Cite

show abstract

“…Such dual repression following DNA methylation would yield net activation of molecular processes that may help maintain memory. Instances of dual repression have been reviewed (Kukushkin and Carew 2017). Fear conditioning increases DNA methylation and decreases expression of the Ser/Thr phosphatases PP1 and calcineurin for, respectively, at least 1 day and as long as 30 days after training (Miller and Sweatt 2007).…”

Section: Dna Methyltransferase Inhibition 24 H After Lts Induction Elmentioning

confidence: 99%

How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory

Smolen¹,

Baxter²,

Byrne³

2019

Learn. Mem.

View full text Add to dashboard Cite

With memory encoding reliant on persistent changes in the properties of synapses, a key question is how can memories be maintained from days to months or a lifetime given molecular turnover? It is likely that positive feedback loops are necessary to persistently maintain the strength of synapses that participate in encoding. Such feedback may occur within signal-transduction cascades and/or the regulation of translation, and it may occur within specific subcellular compartments or within neuronal networks. Not surprisingly, numerous positive feedback loops have been proposed. Some posited loops operate at the level of biochemical signal transduction cascades, such as persistent activation of Ca 2+ /calmodulin kinase II (CaMKII) or protein kinase M ζ. Another level consists of feedback loops involving transcriptional, epigenetic and translational pathways, and autocrine actions of growth factors such as BDNF. Finally, at the neuronal network level, recurrent reactivation of cell assemblies encoding memories is likely to be essential for late maintenance of memory. These levels are not isolated, but linked by shared components of feedback loops. Here, we review characteristics of some commonly discussed feedback loops proposed to underlie the maintenance of memory and long-term synaptic plasticity, assess evidence for and against their necessity, and suggest experiments that could further delineate the dynamics of these feedback loops.We also discuss crosstalk between proposed loops, and ways in which such interaction can facilitate the rapidity and robustness of memory formation and storage. Smolen et al. 3

show abstract

“…As an aversive memory is processed not only during but also after its acquisition, it may be under the influence of modulatory factors until complete stabilization. This dynamic process, referred to as consolidation, demands integrated activity of several brain areas (Izquierdo, Furini, & Myskiw, ; Kukushkin & Carew, ). Preclinical studies investigating how the activity of a discrete brain region contributes to aversive memory consolidation and related synaptic plasticity are of scientific relevance because they provide new insights into brain structure‐function relationships.…”

Section: Introductionmentioning

confidence: 99%

Nucleus reuniens of the thalamus controls fear memory intensity, specificity and long‐term maintenance during consolidation

2018

View full text Add to dashboard Cite

The thalamic nucleus reuniens (NR) has been shown to support bidirectional medial prefrontal cortex-hippocampus communication and synchronization relevant for cognitive processing. Using non-selective or prolonged inactivation of the NR, previous studies reported its activity positively modulates aversive memory consolidation. Here we examined the NR's role in consolidating contextual fear memories with varied strength, at both recent and more remote time points, using muscimol-induced temporary inactivation in rats. Results indicate the NR negatively modulates fear memory intensity, specificity, and long-term maintenance. The more intense, generalized, and enduring fear memory induced by NR inactivation during consolidation was less prone to behavioral suppression by extinction or reconsolidation disruption induced by clonidine, an alpha-2 adrenergic receptor agonist. Lastly, we used immunohistochemistry for Arc protein, which is involved in synaptic modifications underlying memory consolidation, to investigate whether treatment condition and/or conditioning status could change its levels not only in the NR, but also in the hippocampus (dorsal and ventral CA1 subregions) and the medial prefrontal cortex (anterior cingulate, prelimbic and infralimbic subregions). Results indicate a significant imbalance in the number of Arc-expressing neurons in the brain areas investigated in muscimol fear conditioned animals when compared with controls. Collectively, present results provide convergent evidence for the NR's role as a hub regulating quantitative and qualitative aspects of a contextual fear memory during its consolidation that seem to influence the subsequent susceptibility to experimental interventions aiming at attenuating its expression. They also indicate the selectivity and duration of a given inactivation approach may influence its outcomes.

show abstract

Memory Takes Time

Cited by 54 publications

References 199 publications

Sleep and synaptic down‐selection

Sleep and synaptic down‐selection

How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory

Nucleus reuniens of the thalamus controls fear memory intensity, specificity and long‐term maintenance during consolidation

Contact Info

Product

Resources

About