Evidence map›Paper›PMID 41086982›Full record

ArticleJournal of advanced research2026

A ventral hippocampus-basolateral amygdala circuit regulates the unconditioned stimulus retrieval-induced reconsolidation of remote fear memory.

Dan Guo, Zhong Wang, Fanglin Liu, Wenhao Chen, Xuejiao Gao, Shihao Huang, Serik Tabarak, Yuan Yao, Shiya Zhang, Jie Shi and 2 more

Abstract read
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Dan GuoDepartment of Neurobiology, School of Basic Medical Sciences, National Institute on Drug Dependence, Peking University, Beijing 100191, China; Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Zhong WangPeking University Sixth Hospital, Peking University Institute of Mental Health, NHC Key Laboratory of Mental Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), Beijing 100191, China.
Fanglin LiuDepartment of Neurobiology, School of Basic Medical Sciences, National Institute on Drug Dependence, Peking University, Beijing 100191, China; Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Wenhao ChenDepartment of Psychiatry, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou 310003, China.
Xuejiao GaoPeking University Sixth Hospital, Peking University Institute of Mental Health, NHC Key Laboratory of Mental Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), Beijing 100191, China.
Shihao HuangDepartment of Neurobiology, School of Basic Medical Sciences, National Institute on Drug Dependence, Peking University, Beijing 100191, China; Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Serik TabarakPeking-Tsinghua Center for Life Sciences and PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China.
Yuan YaoDepartment of Neurobiology, School of Basic Medical Sciences, National Institute on Drug Dependence, Peking University, Beijing 100191, China; Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Shiya ZhangDepartment of Neurobiology, School of Basic Medical Sciences, National Institute on Drug Dependence, Peking University, Beijing 100191, China; Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Jie ShiDepartment of Neurobiology, School of Basic Medical Sciences, National Institute on Drug Dependence, Peking University, Beijing 100191, China; Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China. Electronic address: shijie@bjmu.edu.cn.
Lin LuPeking University Sixth Hospital, Peking University Institute of Mental Health, NHC Key Laboratory of Mental Health (Peking University), National Clinical Research Center for Mental Disorders (Peking University Sixth Hospital), Beijing 100191, China; Peking-Tsinghua Center for Life Sciences and PKU-IDG/McGovern Institute for Brain Research, Peking University, Beijing 100871, China; Research Unit of Diagnosis and Treatment of Mood Cognitive Disorder, Chinese Academy of Medical Sciences (No.2018RU006), China. Electronic address: linlu@bjmu.edu.cn.
Ying HanDepartment of Neurobiology, School of Basic Medical Sciences, National Institute on Drug Dependence, Peking University, Beijing 100191, China; Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China. Electronic address: yinghan@bjmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionMemory is retrieved and updated during reconsolidation, which provides a potential target for therapeutic intervention. Reconsolidation blockade following unconditioned stimulus (US) retrieval has shown increasing promise in disrupting persistent remote fear memory, yet the underlying neural mechanisms remain poorly understood.

objectivesThis study aims to elucidate the neural mechanisms involved in US retrieval-induced reconsolidation of remote fear memory.

methodsWe established a rat model of contextual fear conditioning to investigate recent and remote fear memory with reconsolidation induced by US or conditioned stimulus (CS) retrieval. Pharmacological intervention, retrograde tracing, immunofluorescence, fiber photometry, as well as chemogenetic manipulation were employed to identify and manipulate key circuits involved in reconsolidation of fear memory.

resultsIn this study, we show that pharmacological disruption of the US retrieval-induced reconsolidation of fear memory had a relatively long-lasting effect and was also effective for remote fear memory. We further reveal that activity of ventral hippocampal CA1 (vCA1)-basolateral amygdala (BLA) circuit specially contributes to US retrieval-induced reconsolidation of remote fear memory. Specifically, pharmacological interventions and inhibition of this circuit after US retrieval effectively disrupted remote fear memory, which showed long-term efficacy and resistance to reinstatement. Conversely, activating this circuit blocked the disruptive effect of propranolol on the remote fear memory reconsolidation.

conclusionOur findings suggest that the vCA1-BLA circuit becomes increasingly important for remote fear memory reconsolidation, particularly induced by US retrieval. This study highlights the potential for targeting specific circuits involved in reconsolidation of remote fear memory for therapeutic interventions in fear-related disorders.

Indexed as

Basolateral Nuclear ComplexFearHippocampusMemory ConsolidationAnimalsConditioning, ClassicalMaleMemoryPropranololRatsRats, Sprague-DawleyPropranololBasolateral amygdalaPTSDReconsolidationRemote fear memoryUnconditioned stimulus retrievalVentral hippocampus

Identifiers

PMID41086982
PMCPMC13316356

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.