Evidence map›Paper›PMID 39848871›Full record

ArticleBritish journal of anaesthesia2025

Sprouting sympathetic fibres release CXCL16 and norepinephrine to synergistically mediate sensory neuronal hyperexcitability in a rodent model of neuropathic pain.

Chen Wang, Anjie Di, Yan Wu, Meng Liu, Ming Wei, Zhengkai Liang, Feng Liu, Haiting Fan, Bo Dong, Changlin Li and 3 more

Abstract read
In one paragraph

Article in British journal of anaesthesia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Trial
  2. Review
  3. Article
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  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

13 authors.

Chen WangDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Anjie DiNeuroscience Program, Zhongshan School of Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China; Guangdong Province Key Laboratory of Brain Function and Disease, Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Yan WuDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Meng LiuDepartment of Anesthesia and Pain Medicine, Guangzhou First People's Hospital, Guangzhou, China.
Ming WeiDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Zhengkai LiangDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Feng LiuYichang Humanwell Pharmaceutical Co., Ltd, Yichang, Hubei, China.
Haiting FanDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Bo DongNeuroscience Program, Zhongshan School of Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China; Guangdong Province Key Laboratory of Brain Function and Disease, Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Changlin LiGuangdong Institute of Intelligence Science and Technology, Zhuhai, China. Electronic address: licl@gdiist.cn.
Ting XuNeuroscience Program, Zhongshan School of Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China. Electronic address: xuting8@mail.sysu.edu.cn.
Wenjun XinNeuroscience Program, Zhongshan School of Medicine, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai, China; Guangdong Province Key Laboratory of Brain Function and Disease, Department of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China. Electronic address: xinwj@mail.sysu.edu.cn.
Xia FengDepartment of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China. Electronic address: fengxia@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic neuropathic pain generally has a poor response to treatment with conventional drugs. Sympathectomy can alleviate neuropathic pain in some patients, suggesting that abnormal sympathetic-somatosensory signaling interactions might underlie some forms of neuropathic pain. The molecular mechanisms underlying sympathetic-somatosensory interactions in neuropathic pain remain obscure.

methodsLumbar sympathectomy was performed in spared nerve injury (SNI) mice or rats, and the up-down method was used to measure the mechanical paw withdrawal threshold. Dorsal root ganglia (DRG) injection and perfusion were used to deliver virus or drugs. Methylated RNA immunoprecipitation sequencing, RNA-sequencing, and immunoelectron microscopy were used to identify neurotransmitters.

resultsWe found that sprouting tyrosine hydroxylase-positive sympathetic fibres in DRG mediated the maintenance of mechanical allodynia after SNI (day 28, P<0.001). We further found that SNI significantly increased the N

conclusionsNorepinephrine and CXCL16 co-released from sympathetic nerve terminals in the DRG synergistically contribute to maintenance of neuropathic pain in a rodent model.

Indexed as

Adrenergic FibersNeuralgiaNorepinephrineSensory Receptor CellsAnimalsDisease Models, AnimalGanglia, SpinalHyperalgesiaMaleMiceMice, Inbred C57BLRatsRats, Sprague-DawleySympathectomyNorepinephrinechronic neuropathic painCXC motif chemokine ligand 16N(6)-methyladenosinenorepinephrinesympathetic ganglion

Identifiers

PMID39848871
PMCPMC11867076

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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.