Evidence map›Paper›PMID 36377439›Full record

ArticleeLife2022

Cellular mechanisms underlying central sensitization in a mouse model of chronic muscle pain.

Yu-Ling Lin, Zhu-Sen Yang, Wai-Yi Wong, Shih-Che Lin, Shuu-Jiun Wang, Shih-Pin Chen, Jen-Kun Cheng, Hui Lu, Cheng-Chang Lien

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
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

13 citing papers in PubMed, 15 citations in OpenAlex.

  1. Review
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  8. Sex differences in the transition to chronic pain.The Journal of clinical investigation · 2025
    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

9 authors at 3 institutions in 2 countries.

Yu-Ling LinInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Zhu-Sen YangInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Wai-Yi WongInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Shih-Che LinInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Shuu-Jiun WangInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Shih-Pin ChenInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.
Jen-Kun ChengDepartment of Medicine, MacKay Medical College, New Taipei, Taiwan.ORCID 0000-0003-2384-7856
Hui LuDepartment of Pharmacology and Physiology, George Washington University, Washington, United States.
Cheng-Chang LienInstitute of Neuroscience, National Yang Ming Chiao Tung University, Taipei, Taiwan.ORCID 0000-0002-6692-9942
National Yang Ming Chiao Tung University · TWGeorge Washington University · USMackay Memorial Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pain disorders are often associated with negative emotions, including anxiety and depression. The central nucleus of the amygdala (CeA) has emerged as an integrative hub for nociceptive and affective components during central pain development. Prior adverse injuries are precipitating factors thought to transform nociceptors into a primed state for chronic pain. However, the cellular basis underlying the primed state and the subsequent development of chronic pain remains unknown. Here, we investigated the cellular and synaptic alterations of the CeA in a mouse model of chronic muscle pain. In these mice, local infusion of pregabalin, a clinically approved drug for fibromyalgia and other chronic pain disorders, into the CeA or chemogenetic inactivation of the somatostatin-expressing CeA (CeA-SST) neurons during the priming phase prevented the chronification of pain. Further, electrophysiological recording revealed that the CeA-SST neurons had increased excitatory synaptic drive and enhanced neuronal excitability in the chronic pain states. Finally, either chemogenetic inactivation of the CeA-SST neurons or pharmacological suppression of the nociceptive afferents from the brainstem to the CeA-SST neurons alleviated chronic pain and anxio-depressive symptoms. These data raise the possibility of targeting treatments to CeA-SST neurons to prevent central pain sensitization.

Indexed as

Chronic PainNeuralgiaAmygdalaAnimalsCentral Nervous System SensitizationDisease Models, AnimalMiceMyalgiaRatsRats, Sprague-Dawleyamygdalacentral sensitizationchronic muscle painmouseneurosciencesomatostatin

Identifiers

PMID36377439
PMCPMC9665847
OpenAlexW4308963284

What OpenQuestion holds

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LicenceCC BY
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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 OpenQuestion graph.