Evidence map›Paper›PMID 28842814›Full record

ArticleJournal of molecular neuroscience : MN2017

Protein Kinase C γ Contributes to Central Sensitization in a Rat Model of Chronic Migraine.

Baixue Wu, Sha Wang, Guangcheng Qin, Jingmei Xie, Ge Tan, Jiying Zhou, Lixue Chen

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular neuroscience : MN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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  5. NMDA and purinergic processes modulate neck muscle activity evoked by noxious stimulation of dura.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2020
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  9. Effect of PKC/NF-Pain research & management · 2020
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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 2 institutions in 1 country.

Baixue WuLaboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Sha WangLaboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Guangcheng QinLaboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Jingmei XieLaboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ge TanChongqing Key Laboratory of Neurology, Chongqing, China.
Jiying ZhouChongqing Key Laboratory of Neurology, Chongqing, China.
Lixue ChenLaboratory Research Center, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. chenlixue@hospital.cqmu.edu.cn.ORCID http://orcid.org/0000-0001-8213-8828
The Affiliated Yongchuan Hospital of Chongqing Medical University · CNChildren's Hospital of Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase C γ (PKCγ) is a critical regulator of central sensitization and is widely recognized to be involved in the pathogenesis of chronic migraine (CM). However, the function of PKCγ in CM remains unknown. This study investigated the role of PKCγ on pathogenesis of CM. We repeated infusions of inflammatory soup (IS) on the intact dura of conscious rats to model recurrent trigeminovascular or dural nociceptor activation assumed to occur in patients with CM. The von Frey test was then used to detect changes in pain threshold. QT-PCR, western blotting, and double immunofluorescence staining were performed to detect the expression and location of PKCγ in the trigeminal nucleus caudalis (TNC) and the expressions of calcitonin gene-related peptide (CGRP), c-Fos, and phosphorylation level of GluR1 subunit at serine 831. Chelerythrine chloride (CHE) and phorbol 12-myristate 13-acetate (PMA) were administrated to investigate the role of PKCγ in central sensitization. We found that repeated infusions of IS induced mechanical allodynia. PKCγ was significantly increased in TNC after CM. Furthermore, inhibition of PKCγ by CHE relieved allodynia and reduced the expression of CGRP and c-Fos. Activation of PKCγ by PMA aggravated allodynia and increased the expression of CGRP and c-Fos. In addition, inhibition of PKCγ reduced the phosphorylation level of GluR1; in contrast, activation of PKCγ increased the phosphorylation level of GluR1. These results suggest PKCγ-induced GluR1 phosphorylation might participate in central sensitization in a rat model of CM. We suggest that PKCγ is a potential therapeutic target for CM.

Indexed as

Central Nervous System SensitizationAnimalsCalcitonin Gene-Related PeptideMaleMigraine DisordersPain ThresholdPhosphorylationProtein Kinase CProtein Processing, Post-TranslationalProto-Oncogene Proteins c-fosRatsRats, Sprague-DawleyReceptors, AMPATrigeminal NucleiCalcitonin Gene-Related PeptideProtein Kinase Cprotein kinase C gammaProto-Oncogene Proteins c-fosReceptors, AMPACentral sensitizationChronic migrainePKC γTrigeminal nucleus caudalis

Identifiers

PMID28842814
OpenAlexW2748549445

What OpenQuestion holds

Textmetadata
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.