Evidence map›Paper›PMID 37561576›Full record

ArticleThe Journal of clinical investigation2023

Nucleus accumbens D1/D2 circuits control opioid withdrawal symptoms in mice.

Yongsheng Zhu, Kejia Wang, Tengfei Ma, Yuanyuan Ji, Yin Lou, Xiaoyu Fu, Ye Lu, Yige Liu, Wei Dang, Qian Zhang and 6 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Article
  2. Kappa opioid receptor-dependent depressive-like behaviors associated with morphine withdrawal contribute to stress-induced reinstatement of morphine seeking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  11. Review
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  14. A Drd1-cre mouse line with nucleus accumbens gene dysregulation exhibits blunted fentanyl seeking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  15. 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

16 authors.

Yongsheng ZhuCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Kejia WangFujian Provincial Key Laboratory of Organ and Tissue Regeneration, Xiamen Key Laboratory of Regeneration Medicine, Organ Transplantation Institute of Xiamen University, School of Medicine, Xiamen University, Xiamen, China.
Tengfei MaSchool of Pharmacy, Nanjing Medical University, Nanjing, China.
Yuanyuan JiCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Yin LouCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Xiaoyu FuCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Ye LuCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Yige LiuCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Wei DangThe Sixth Ward, Xi'an Mental Health Center, Xi'an, China.
Qian ZhangDepartment of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan, China.
Fangyuan YinCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Kena WangCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Bing YuSchool of Pharmacy, Nanjing Medical University, Nanjing, China.
Hongbo ZhangCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Jianghua LaiCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.
Yunpeng WangCollege of Forensic Science, Key Laboratory of National Health Commission for Forensic Science, National Biosafety Evidence Foundation, Xi'an Jiaotong University, Xi'an, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The nucleus accumbens (NAc) is the most promising target for drug use disorder treatment. Deep brain stimulation (DBS) of NAc is effective for drug use disorder treatment. However, the mechanisms by which DBS produces its therapeutic effects remain enigmatic. Here, we define a behavioral cutoff criterion to distinguish depressive-like behaviors and non-depressive-like behaviors in mice after morphine withdrawal. We identified a basolateral amygdala (BLA) to NAc D1 medium spiny neuron (MSN) pathway that controls depressive-like behaviors after morphine withdrawal. Furthermore, the paraventricular nucleus of thalamus (PVT) to NAc D2 MSN pathway controls naloxone-induced acute withdrawal symptoms. Optogenetically induced long-term potentiation with κ-opioid receptor (KOR) antagonism enhanced BLA to NAc D1 MSN signaling and also altered the excitation/inhibition balance of NAc D2 MSN signaling. We also verified that a new 50 Hz DBS protocol reversed morphine withdrawal-evoked abnormal plasticity in NAc. Importantly, this refined DBS treatment effectively alleviated naloxone-induced withdrawal symptoms and depressive-like behaviors and prevented stress-induced reinstatement. Taken together, the results demonstrated that input- and cell type-specific synaptic plasticity underlies morphine withdrawal, which may lead to novel targets for the treatment of opioid use disorder.

Indexed as

Analgesics, OpioidSubstance Withdrawal SyndromeAnimalsMiceMice, Inbred C57BLMorphineNaloxoneNucleus AccumbensReceptors, Dopamine D1Receptors, Dopamine D2Analgesics, OpioidMorphineNaloxoneReceptors, Dopamine D1Receptors, Dopamine D2AddictionDepressionMouse modelsNeuroscience

Identifiers

PMID37561576
PMCPMC10503809

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.