Evidence map›Paper›PMID 41872516›Full record

ArticleMolecular psychiatry2026

Paradoxical role of the mesocorticolimbic Netrin1-DCC pathway in social competition and vulnerability to methamphetamine abuse during adolescence.

Wei Xu, Jiafeng Zhong, Lijie Ding, Haiyang Jing, Xiaoqing Chen, Ting Pan, Baofang Zhang, Ruiyi Zhou, Liang Xu, Jian He and 5 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular psychiatry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

15 authors.

Wei Xu *Faculty of Life and Health Sciences, Shenzhen University of Advanced Technology, Shenzhen, 518055, China. freefresh2000@163.com.ORCID http://orcid.org/0000-0002-7261-9203
Jiafeng Zhong *Shenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Lijie DingFaculty of Life and Health Sciences, Shenzhen University of Advanced Technology, Shenzhen, 518055, China.
Haiyang JingShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Xiaoqing ChenFaculty of Life and Health Sciences, Shenzhen University of Advanced Technology, Shenzhen, 518055, China.
Ting PanFaculty of Life and Health Sciences, Shenzhen University of Advanced Technology, Shenzhen, 518055, China.
Baofang ZhangShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Ruiyi ZhouShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Liang XuShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Jian HeShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Hanhe LiuShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Taian LiuShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Zhonghua LuShenzhen Key Laboratory of Drug Addiction, Shenzhen Neher Neural Plasticity Laboratory, the Brain Cognition and Brain Disease Institute, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Wen ChenGuangdong Provincial Key Laboratory of Food, Nutrition and Health, Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, 510080, China.
Yingjie ZhuFaculty of Life and Health Sciences, Shenzhen University of Advanced Technology, Shenzhen, 518055, China. yj.zhu1@siat.ac.cn.ORCID http://orcid.org/0000-0002-0783-0897

Funding

Guangdong Science and Technology Department (Science and Technology Department, Guangdong Province) 2023A1515012122Guangdong Science and Technology Department (Science and Technology Department, Guangdong Province) 2023B1515040009Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) 2021ZD0202103Shenzhen Science and Technology Innovation Commission KCXFZ20211020164543007Shenzhen Science and Technology Innovation Commission KCXFZ20230731100901004Yunnan Provincial Science and Technology Department (Yunnan Department of Science and Technology) 202305AK340001
6 · The paper itself

Abstract

Social competition exerts a diverse set of influences on neural development and behavior during adolescence and yet the precise underlying molecular mechanisms remain poorly understood. Here, we demonstrate that individual rodents that rank lower in social hierarchies are more vulnerable to drug abuse. Proteomic analysis revealed a crucial role of the mesocorticolimbic netrin-1/DCC/UNC5 pathway within the nucleus accumbens (NAc) in mediating the impact of social competition. We found that mice with a conditional knockout of the deleted in colorectal cancer (DCC) gene in dopamine neurons were more likely to achieve higher social rank but exhibited increased drug-seeking behaviors. Following dopamine fiber immunostaining, these outcomes were attributed to ectopic mesolimbic dopamine fibers, which enhanced risk-taking behavior in winners that had DCC knockout. Collectively, our work elucidates a molecular mechanism through which social competition influences adolescent brain development and behavior, particularly in relation to drug susceptibility.

Indexed as

Amphetamine-Related DisordersAnimalsDCC ReceptorDopamineDopaminergic NeuronsMaleMesolimbic SystemMethamphetamineMiceMice, Inbred C57BLMice, KnockoutNetrin-1Nucleus AccumbensSignal TransductionSocial BehaviorTumor Suppressor ProteinsDcc protein, mouseDCC ReceptorDopamineMethamphetamineNetrin-1Ntn1 protein, mouseTumor Suppressor Proteins

Identifiers

PMID41872516

What Socratic 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 Socratic graph.