Evidence map›Paper›PMID 25057203›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

eIF2α dephosphorylation in basolateral amygdala mediates reconsolidation of drug memory.

Min Jian, Yi-Xiao Luo, Yan-Xue Xue, Ying Han, Hai-Shui Shi, Jian-Feng Liu, Wei Yan, Ping Wu, Shi-Qiu Meng, Jia-Hui Deng and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

39 citing papers in PubMed, 61 citations in OpenAlex.

  1. Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  5. The ISR downstream target ATF4 represses long-term memory in a cell type-specific manner.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  19. Protein Translation and Psychiatric Disorders.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 1 country.

Min JianInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Yi-Xiao LuoInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Yan-Xue XueNational Institute on Drug Dependence, Peking University, Beijing 100191, China.
Ying HanInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Hai-Shui ShiDepartment of Biochemistry and Molecular Biology, Basic Medical College, Hebei Medical University, Shijiazhuang 050017, China, and.
Jian-Feng LiuInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Wei YanInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Ping WuNational Institute on Drug Dependence, Peking University, Beijing 100191, China.
Shi-Qiu MengInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Jia-Hui DengInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Hao-Wei ShenNational Institute on Drug Dependence, Peking University, Beijing 100191, China.
Jie ShiNational Institute on Drug Dependence, Peking University, Beijing 100191, China, linlu@bjmu.edu.cn Shijie@bjmu.edu.cn.
Lin LuInstitute of Mental Health/Peking University Sixth Hospital and Key Laboratory of Mental Health and National Institute on Drug Dependence, Peking University, Beijing 100191, China, Peking-Tsinghua Center for Life Sciences and PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China linlu@bjmu.edu.cn Shijie@bjmu.edu.cn.
Peking University · CNNational Institutes for Food and Drug Control · CNPeking University Sixth Hospital · CNCenter for Life Sciences · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maladaptive memories elicited by exposure to environmental stimuli associated with drugs of abuse are often responsible for relapse among addicts. Interference with the reconsolidation of drug memory can inhibit drug seeking. Previous studies have indicated that the dephosphorylation of the eukaryotic initiation factor 2 α-subunit (eIF2α) plays an important role in synaptic plasticity and long-term memory consolidation, but its role in the reconsolidation of drug memory remains unknown. The amygdala is required for the reconsolidation of a destabilized drug memory after retrieval of drug-paired stimuli. Here, we used conditioned place preference (CPP) and self-administration procedures to determine whether amygdala eIF2α dephosphorylation is required for the reconsolidation of morphine and cocaine memories in rats. We found that the levels of eIF2α phosphorylation (Ser51) and activating transcription factor 4 (ATF4) were decreased after reexposure to a previously morphine- or cocaine-paired context (i.e., a memory retrieval procedure) in the basolateral amygdala (BLA) but not in the central amygdala. Intra-BLA infusions of Sal003, a selective inhibitor of eIF2α dephosphorylation, immediately after memory retrieval disrupted the reconsolidation of morphine- or cocaine-induced CPP, leading to a long-lasting suppression of drug-paired stimulus-induced craving. Advanced knockdown of ATF4 expression in the BLA by lentivirus-mediated short-hairpin RNA blocked the disruption of the reconsolidation of morphine-induced CPP induced by Sal003 treatment. Furthermore, inhibition of eIF2α dephosphorylation in the BLA immediately after light/tone stimulus retrieval decreased subsequent cue-induced heroin-seeking behavior in the self-administration procedure. These results demonstrate that eIF2α dephosphorylation in the BLA mediates the memory reconsolidation of drug-paired stimuli.

Indexed as

CuesAmygdalaAnimalsCocaineDrug-Seeking BehaviorEukaryotic Initiation Factor-2HeroinMaleMemoryMorphinePhosphorylationRatsRats, Sprague-DawleySelf AdministrationCocaineEukaryotic Initiation Factor-2HeroinMorphine

Identifiers

PMID25057203
PMCPMC6608301
OpenAlexW1991170680

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.