Evidence map›Paper›PMID 26515544›Full record

ArticleScientific reports2015

Phosphorylation of NR2B NMDA subunits by protein kinase C in arcuate nucleus contributes to inflammatory pain in rats.

Fan Bu, Huiyu Tian, Shan Gong, Qi Zhu, Guang-Yin Xu, Jin Tao, Xinghong Jiang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
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  13. Remembering Mechanosensitivity of NMDA Receptors.Frontiers in cellular neuroscience · 2019
    Review
  14. Article
  15. Article
  16. Article
  17. Neuroanatomical characterization of imidazoline IThe European journal of neuroscience · 2018
    Article
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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

7 authors at 1 institution in 1 country.

Fan BuKey Laboratory of Pain Basic Research and Clinical Therapy, Department of Physiology &Neurobiology, Medical College of Soochow University, Suzhou 215123, P.R. China.
Huiyu TianKey Laboratory of Pain Basic Research and Clinical Therapy, Department of Physiology &Neurobiology, Medical College of Soochow University, Suzhou 215123, P.R. China.
Shan GongKey Laboratory of Pain Basic Research and Clinical Therapy, Department of Physiology &Neurobiology, Medical College of Soochow University, Suzhou 215123, P.R. China.
Qi ZhuKey Laboratory of Pain Basic Research and Clinical Therapy, Department of Physiology &Neurobiology, Medical College of Soochow University, Suzhou 215123, P.R. China.
Guang-Yin XuKey Laboratory of Pain Basic Research and Clinical Therapy, Department of Physiology &Neurobiology, Medical College of Soochow University, Suzhou 215123, P.R. China.
Jin TaoKey Laboratory of Pain Basic Research and Clinical Therapy, Department of Physiology &Neurobiology, Medical College of Soochow University, Suzhou 215123, P.R. China.
Xinghong JiangKey Laboratory of Pain Basic Research and Clinical Therapy, Department of Physiology &Neurobiology, Medical College of Soochow University, Suzhou 215123, P.R. China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The arcuate nucleus (ARC) of the hypothalamus plays a key role in pain processing. Although it is well known that inhibition of NMDA receptor (NMDAR) in ARC attenuates hyperalgesia induced by peripheral inflammation, the underlying mechanism of NMDAR activation in ARC remains unclear. Protein kinase C (PKC) is involved in several signalling cascades activated in physiological and pathological conditions. Therefore, we hypothesised that upregulation of PKC activates NMDARs in the ARC, thus contributing to inflammatory hyperalgesia. Intra-ARC injection of chelerythrine (CC), a specific PKC inhibitor, attenuated complete Freund's adjuvant (CFA) induced thermal and mechanical hyperalgesia in a dose-dependent manner. In vivo extracellular recordings showed that microelectrophoresis of CC or MK-801 (a NMDAR antagonist) significantly reduced the enhancement of spontaneous discharges and pain-evoked discharges of ARC neurons. In addition, CFA injection greatly enhanced the expression of total and phosphorylated PKCγ in the ARC. Interestingly, CFA injection also remarkably elevated the level of phosphorylated NR2B (Tyr1472) without affecting the expression of total NR2B. Importantly, intra-ARC injection of CC reversed the upregulation of phosphorylated NR2B subunits in the ARC. Taken together, peripheral inflammation leads to an activation of NMDARs mediated by PKC activation in the ARC, thus producing thermal and mechanical hyperalgesia.

Indexed as

AnimalsArcuate Nucleus of HypothalamusBehavior, AnimalBenzophenanthridinesDisease Models, AnimalDizocilpine MaleateEvoked PotentialsFreund's AdjuvantHyperalgesiaMaleNeuronsPhosphorylationProtein Kinase CProtein SubunitsRatsRats, Sprague-DawleyBenzophenanthridineschelerythrineDizocilpine MaleateFreund's AdjuvantProtein Kinase CProtein SubunitsReceptors, N-Methyl-D-Aspartate

Identifiers

PMID26515544
PMCPMC4626761
OpenAlexW2411932383

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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.