Evidence map›Paper›PMID 40013979›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

Prefrontal FGF1 Signaling is Required for Accumbal Deep Brain Stimulation Treatment of Addiction.

Wan-Kun Gong, Xue Li, Le Wang, Qian Yang, Alix Tiran-Cappello, Zhichao Liang, James Samsom, Quanying Liu, He Lin, Christelle Baunez and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
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.

Wan-Kun GongShanghai Key Laboratory of Psychotic Disorders, Brain Health Institute, National Center for Mental Disorders, Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine and School of Psychology, Shanghai, 200030, China.ORCID https://orcid.org/0009-0004-1641-191X
Xue LiDepartment of Clinical Laboratory Diagnosis, Changhai Hospital, Shanghai, 200433, China.
Le WangInstitute of Mental Health and Drug Discovery, Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine Vision and Brain Health), School of Mental Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Qian YangShanghai Key Laboratory of Psychotic Disorders, Brain Health Institute, National Center for Mental Disorders, Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine and School of Psychology, Shanghai, 200030, China.
Alix Tiran-CappelloInstitut de Neurosciences de la Timone, UMR7289 CNRS & Aix-Marseille Université, Marseille, France.
Zhichao LiangShenzhen Key Laboratory of Smart Healthcare Engineering, Department of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, 518055, China.
James SamsomCampbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, M5T1R8, Canada.
Quanying LiuShenzhen Key Laboratory of Smart Healthcare Engineering, Department of Biomedical Engineering, Southern University of Science and Technology, Shenzhen, 518055, China.
He LinThe Third Research Institute of Ministry of Public Security, Shanghai, 200438, China.
Christelle BaunezInstitut de Neurosciences de la Timone, UMR7289 CNRS & Aix-Marseille Université, Marseille, France.
Fang LiuInstitute of Mental Health and Drug Discovery, Oujiang Laboratory (Zhejiang Lab for Regenerative Medicine Vision and Brain Health), School of Mental Health, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Ti-Fei YuanShanghai Key Laboratory of Psychotic Disorders, Brain Health Institute, National Center for Mental Disorders, Shanghai Mental Health Center, Shanghai Jiaotong University School of Medicine and School of Psychology, Shanghai, 200030, China.ORCID https://orcid.org/0000-0003-0510-715X

Funding

China Postdoctoral Science Foundation 2022M712126International Science and Technology Cooperation Programme 82461160261Major Research Plan T2394535National Natural Science Foundation of China 32100895National Natural Science Foundation of China 32241015National Outstanding Youth Science Fund Project of National Natural Science Foundation of China 82325019Science and Technology Commission of Shanghai Municipality 23XD1423000Science and Technology Commission of Shanghai Municipality 23ZR1480800Shanghai Municipal Commission of Health 2022JC016Shanghai Municipal Education Commission 20181715
6 · The paper itself

Abstract

Deep brain stimulation (DBS) has emerged as a prospective treatment for psychiatric disorders; for example, DBS targeting the nucleus accumbens (NAc) abolishes addictive behaviors. However, neither the core pathway nor the cellular mechanisms underlying these therapeutic effects are known. Here, morphine-induced conditioned place preference (CPP) in mice as an addiction model and NAc-DBS combined with adeno-associated virus gene delivery for activity-dependent tagging, transgenic and chemogenetic manipulation of recruited neuronal networks are used. It is reported that a cortical-accumbal pathway and local fibroblast growth factor 1 (FGF1) signaling in the medial prefrontal cortex (mPFC) are critical for NAc-DBS to be effective in altering morphine CPP. It is shown that NAc-DBS retrogradely activates mPFC neurons projecting to the NAc, and chemogenetic activation/inhibition of these DBS-activated neuron ensembles in the mPFC reproduces the NAc-DBS effects on CPP. Sustained therapeutic effects accompany reductions in local FGF1 binding to fibroblast growth factor receptor 1 (FGFR1) in these neurons. Additionally, overexpressing FGF1 in the mPFC-NAc pathway abolishes the therapeutic effects of NAc-DBS. These results demonstrate that the mPFC-NAc pathway forms a top-down motif to regulate the therapeutic effects of subcortical DBS on addiction. These results support the potential for addiction treatments involving FGF1 signaling and highlight the mPFC as a target for noninvasive brain stimulation.

Indexed as

Behavior, AddictiveDeep Brain StimulationFibroblast Growth Factor 1Nucleus AccumbensPrefrontal CortexAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLSignal TransductionFibroblast Growth Factor 1addictiondeep brain stimulationnucleus accumbensprefrontal cortex

Identifiers

PMID40013979
PMCPMC12021060

What OpenQuestion holds

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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.