Evidence map›Paper›PMID 34111331›Full record

ArticleCNS neuroscience & therapeutics2021

Spinal microglial β-endorphin signaling mediates IL-10 and exenatide-induced inhibition of synaptic plasticity in neuropathic pain.

Le Ma, Shiyu Peng, Jinbao Wei, Mengjing Zhao, Khalil Ali Ahmad, Jinghong Chen, Yong-Xiang Wang

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Glial cells in neuropathic pain.Physiological reviews · 2026
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  15. Article
  16. Neuroplasticity in the transition from acute to chronic pain.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  17. Article
  18. Article
  19. Synapse Regulation.Advances in neurobiology · 2024
    Review
  20. Review
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

7 authors at 1 institution in 1 country.

Le MaKing's Lab, Shanghai Jiao Tong University School of Pharmacy, Shanghai, China.
Shiyu PengShanghai Key Laboratory of Psychotic Disorders, Shanghai Jiao Tong University School of Medicine, Shanghai Mental Health Center, Shanghai, China.
Jinbao WeiKing's Lab, Shanghai Jiao Tong University School of Pharmacy, Shanghai, China.
Mengjing ZhaoKing's Lab, Shanghai Jiao Tong University School of Pharmacy, Shanghai, China.
Khalil Ali AhmadKing's Lab, Shanghai Jiao Tong University School of Pharmacy, Shanghai, China.
Jinghong ChenShanghai Key Laboratory of Psychotic Disorders, Shanghai Jiao Tong University School of Medicine, Shanghai Mental Health Center, Shanghai, China.
Yong-Xiang WangKing's Lab, Shanghai Jiao Tong University School of Pharmacy, Shanghai, China.ORCID 0000-0001-5557-0076
Shanghai Jiao Tong University · CN

Funding

Yangzi River Pharmaceuticals Group
6 · The paper itself

Abstract

aimThis study aimed to investigate the regulation of pain hypersensitivity induced by the spinal synaptic transmission mechanisms underlying interleukin (IL)-10 and glucagon-like peptide 1 receptor (GLP-1R) agonist exenatide-induced pain anti-hypersensitivity in neuropathic rats through spinal nerve ligations.

methodsNeuropathic pain model was established by spinal nerve ligation of L5/L6 and verified by electrophysiological recording and immunofluorescence staining. Microglial expression of β-endorphin through autocrine IL-10- and exenatide-induced inhibition of glutamatergic transmission were performed by behavioral tests coupled with whole-cell recording of miniature excitatory postsynaptic currents (mEPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) through application of endogenous and exogenous IL-10 and β-endorphin.

resultsIntrathecal injections of IL-10, exenatide, and the μ-opioid receptor (MOR) agonists β-endorphin and DAMGO inhibited thermal hyperalgesia and mechanical allodynia in neuropathic rats. Whole-cell recordings of bath application of exenatide, IL-10, and β-endorphin showed similarly suppressed enhanced frequency and amplitude of the mEPSCs in the spinal dorsal horn neurons of laminae II, but did not reduce the frequency and amplitude of mIPSCs in neuropathic rats. The inhibitory effects of IL-10 and exenatide on pain hypersensitive behaviors and spinal synaptic plasticity were totally blocked by pretreatment of IL-10 antibody, β-endorphin antiserum, and MOR antagonist CTAP. In addition, the microglial metabolic inhibitor minocycline blocked the inhibitory effects of IL-10 and exenatide but not β-endorphin on spinal synaptic plasticity.

conclusionThis suggests that spinal microglial expression of β-endorphin mediates IL-10- and exenatide-induced inhibition of glutamatergic transmission and pain hypersensitivity via presynaptic and postsynaptic MORs in spinal dorsal horn.

Indexed as

Interleukin-10MicrogliaAnalgesics, OpioidAnimalsBehavior, Animalbeta-EndorphinEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Excitatory Postsynaptic PotentialsExenatideGlutamic AcidInjections, SpinalNeuralgiaNeuronal PlasticityPatch-Clamp TechniquesRatsReceptors, Opioid, muAnalgesics, Opioidbeta-EndorphinEnkephalin, Ala(2)-MePhe(4)-Gly(5)-ExenatideGlutamic AcidIL10 protein, humanInterleukin-10Receptors, Opioid, muexenatideIL-10mEPSCsmicrogliamIPSCsNeuropathic painβ-endorphin

Identifiers

PMID34111331
PMCPMC8446220
OpenAlexW3167595114

What OpenQuestion holds

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LicenceCC BY
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 OpenQuestion graph.