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Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories

ABSTRACT: Remembrances of traumata range among the most enduring forms of memories. Despite the elevated lifetime prevalence of anxiety disorders, effective strategies to attenuate long-term traumatic memories are scarce. The most efficacious treatments to diminish recent (i.e., day-old) traumata capitalize on memory updating mechanisms during reconsolidation that are initiated upon memory recall. Here, we show that in mice successful reconsolidation-updating paradigms for recent memories fail to attenuate remote (i.e., month-old) ones. We find that whereas recent memory recall induces a limited period of hippocampal neuroplasticity mediated, in part, by S-nitrosylation of HDAC2 and histone acetylation, such plasticity is absent for remote memories. However, by using an HDAC2-targeting inhibitor (HDACi) during reconsolidation, even remote memories can be persistently attenuated. This intervention epigenetically primes the expression of neuroplasticity-related genes as revealed by whole genome RNA sequencing, which is accompanied by higher metabolic, synaptic and structural plasticity. Thus, applying HDACis during memory reconsolidation might constitute a treatment option for remote traumata.

ORGANISM(S): Mus musculus

PROVIDER: GSE53794 | GEO | 2014/01/04

SECONDARY ACCESSION(S): PRJNA233306

REPOSITORIES: GEO

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Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories

Project description:Remembrances of traumata range among the most enduring forms of memories. Despite the elevated lifetime prevalence of anxiety disorders, effective strategies to attenuate long-term traumatic memories are scarce. The most efficacious treatments to diminish recent (i.e., day-old) traumata capitalize on memory updating mechanisms during reconsolidation that are initiated upon memory recall. Here, we show that in mice successful reconsolidation-updating paradigms for recent memories fail to attenuate remote (i.e., month-old) ones. We find that whereas recent memory recall induces a limited period of hippocampal neuroplasticity mediated, in part, by S-nitrosylation of HDAC2 and histone acetylation, such plasticity is absent for remote memories. However, by using an HDAC2-targeting inhibitor (HDACi) during reconsolidation, even remote memories can be persistently attenuated. This intervention epigenetically primes the expression of neuroplasticity-related genes as revealed by whole genome RNA sequencing, which is accompanied by higher metabolic, synaptic and structural plasticity. Thus, applying HDACis during memory reconsolidation might constitute a treatment option for remote traumata. 3 biological replicates per group were analyzed. The material analyzed was whole hippocampi from one brain hemisphere, from which total RNA was extracted.

2014-01-04 | E-GEOD-53794 | biostudies-arrayexpress

Mus musculus

Project description:Epigenetic priming of memory updating during reconsolidation to attenuate remote fear memories

| PRJNA233306 | ENA

Primary cilia are required for the persistence of memory and stabilization of perineuronal nets

Project description:We investigate the gene expression changes occurring during the transition of aversive episodic memories from recent to remote. Early mechanisms of memory formation (synaptic consolidation) have been extensively characterized. However, delayed mechanisms (systems consolidation), which maintain hippocampal activity as memories stabilize in cortical circuits, are not well understood. Transcriptomic analysis reveals that, contrary to the transient expression of early- and delayed-response genes, the expression of cytoskeleton- and extracellular matrix- associated genes remains dynamic even at remote time points. The most profound expression changes clustered around primary cilium-associated and collagen genes.

2021-06-05 | GSE174076 | GEO

RNA sequencing from neural ensembles activated during fear conditioning in the mouse temporal association cortex

Project description:The stable formation of remote fear memories is thought to require neuronal gene induction in cortical ensembles that are activated during learning. However, the set of genes expressed specifically in these activated ensembles is not known; knowledge of such transcriptional profiles may offer insights into the molecular program underlying stable memory formation. Here we use RNA-Seq to identify genes whose expression is enriched in activated cortical ensembles labeled during associative fear learning. We first establish that mouse temporal association cortex (TeA) is required for remote recall of auditory fear memories. We then perform RNA-Seq in TeA neurons that are labeled by the activity reporter Arc-dVenus during learning. We identify 944 genes with enriched expression in Arc-dVenus+ neurons. These genes include markers of L2/3, L5b, and L6 excitatory neurons but not glial or inhibitory markers, confirming Arc-dVenus to be an excitatory neuron-specific, layer non-specific activity reporter. Cross comparisons to other transcriptional profiles show that 125 of the enriched genes are also activity-regulated in vitro or induced by visual stimulus in the visual cortex, suggesting that they may be induced generally in the cortex in an experience-dependent fashion. Prominent among the enriched genes are those encoding potassium channels that down-regulate neuronal activity, suggesting the possibility that part of the molecular program induced by fear conditioning may initiate homeostatic plasticity.

2016-08-31 | GSE85128 | GEO

Remote memory and cortical synaptic plasticity require neuronal CCCTC-binding factor (CTCF), a central organizer of 3D chromatin architecture

Project description:Molecular mechanism of long-term memory has been extensively studied in the context of hippocampus-dependent recent memory examined within several days; however, months-old remote memory maintained in the cortex for long-term has not much been investigated at molecular levels yet. Various epigenetic mechanisms are known to be important for long-term memory, but how 3D chromatin architecture and its regulator molecules contribute to neuronal plasticity and memory consolidation are still largely unknown. To assess memory upon perturbation of 3D chromatin structure, we chose CCCTC-binding factor (CTCF), a seven-zinc finger protein well known for its role as a transcription factor and a chromatin regulator, and created the conditional knockout (cKO) mice, in which CTCF is lost in neurons during adulthood. Our CTCF cKO mice showed normal recent memory in contextual fear conditioning and spatial water maze task. However, they showed remarkable impairments in remote memory in both tasks. Underlying the remote memory-specific phenotypes, we found that loss of CTCF disrupts cortical long-term potentiation (LTP) but not hippocampal LTP. Through RNA-sequencing, we found that CTCF KD cultured cortical neurons have altered the expression of hundreds of genes, some of which we uncovered to be regulated by neuronal activity. These results suggest that remote memory storage in the cortex requires CTCF-mediated chromatin regulation in neurons while recent memory formation in the hippocampus does not.

2018-05-21 | GSE99230 | GEO

Identification of the Similarities and Differences of Molecular Networks Associated With Fear Memory Formation, Extinction, and Updating in the Amygdala [circRNA-seq]

Project description:circRNA sequencing for 6 samples. In this study, we systematically observed the expression of mRNAs, microRNAs (miRNA), long non-coding RNAs (lncRNAs), and circRNAs in the basolateral amygdala of mice after fear memory formation, extinction, and updating by whole-transcriptional sequencing, then a variety of inter-group comparison and bioinformatics analysis were used to find the differential expressed RNAs, enrich the function of them, and construct the molecular interaction networks. Moreover, competing endogenous RNA (ceRNA) molecular networks and transcriptional regulatory networks for the candidate circRNAs were constructed. Through these analyses, we found that about 10% of molecules were both involved in the fear memory extinction and formation, but the molecules and their signaling pathways were almost completely different between fear memory extinction and updating. This study describes a relatively detailed molecular network for fear memory updating, which might provide some novel directions for further mechanism research, and help to develop a specific physical method for fear memory intervention, based on the regulation of these key molecules.

2022-01-07 | GSE185806 | GEO

Identification of the Similarities and Differences of Molecular Networks Associated With Fear Memory Formation, Extinction, and Updating in the Amygdala

Project description:In this study, we systematically observed the expression of mRNAs, microRNAs (miRNA), long non-coding RNAs (lncRNAs), and circRNAs in the basolateral amygdala of mice after fear memory formation, extinction, and updating by whole-transcriptional sequencing, then a variety of inter-group comparison and bioinformatics analysis were used to find the differential expressed RNAs, enrich the function of them, and construct the molecular interaction networks. Moreover, competing endogenous RNA (ceRNA) molecular networks and transcriptional regulatory networks for the candidate circRNAs were constructed. Through these analyses, we found that about 10% of molecules were both involved in the fear memory extinction and formation, but the molecules and their signaling pathways were almost completely different between fear memory extinction and updating. This study describes a relatively detailed molecular network for fear memory updating, which might provide some novel directions for further mechanism research, and help to develop a specific physical method for fear memory intervention, based on the regulation of these key molecules.

2022-01-07 | GSE185808 | GEO

Identification of the Similarities and Differences of Molecular Networks Associated With Fear Memory Formation, Extinction, and Updating in the Amygdala [miRNA-seq]

2022-01-07 | GSE185807 | GEO

Characteristics of medial prefrontal cortex during retrieval of METH-associated CPP memory

Project description:To investigate the candidate molecular mechanisms underlies methamphetamine-associated CPP memory retrieval and reconsolidation, we compared the transcriptional profling changes in the mPFC between mice that underwent retrieval and non-retrieval after methamphetamine-paired CPP training.

2024-04-26 | GSE249153 | GEO

Synaptically recruited lncRNA SLAMR facilitates structural plasticity in fear memory consolidation by modulatin translation

Project description:LncRNAs are involved in critical processes for cell homeostasis and function. However, it remains largely unknown whether and how the transcriptional regulation of long noncoding RNAs results in activity-dependent changes at the synapse and facilitate formation of long-term memories. Here, we report the identification of a novel lncRNA, SLAMR, that becomes enriched in CA1- but not in CA3-hippocampal neurons upon contextual fear conditioning. SLAMR is transported to dendrites via the molecular motor KIF5C and recruited to the synapse in response to stimulation. Loss of function of SLAMR reduced dendritic complexity and impaired activity-dependent changes in spine structural plasticity. Interestingly, the gain of function of SLAMR enhanced dendritic complexity, and spine density through enhanced translation. Analyses of the SLAMR interactome revealed its association with CaMKIIa protein through a 220-nucleotide element and its modulation of CaMKIIa activity. Furthermore, loss-of-function of SLAMR in CA1 selectively impairs consolidation but neither acquisition, recall, nor extinction of fear memory and spatial memory. Together, these results establish a new mechanism for activity dependent changes at the synapse and consolidation of contextual fear memory.

2023-03-13 | MSV000091477 | MassIVE

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