Evidence map›Paper›PMID 15537893›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Role of mitogen-activated protein kinase activation in injured and intact primary afferent neurons for mechanical and heat hypersensitivity after spinal nerve ligation.

Koichi Obata, Hiroki Yamanaka, Kimiko Kobayashi, Yi Dai, Toshiyuki Mizushima, Hirokazu Katsura, Tetsuo Fukuoka, Atsushi Tokunaga, Koichi Noguchi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed
9.2field-weighted citation impact, top 1% 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

133 citing papers in PubMed, 310 citations in OpenAlex.

  1. Glial cells in neuropathic pain.Physiological reviews · 2026
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  10. A journey from molecule to physiology andFrontiers in pharmacology · 2023
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  16. C-Jun N-Terminal Kinase Post-Translational Regulation of Pain-Related Acid-Sensing Ion Channels 1b and 3.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  17. Rapamycin reduces orofacial nociceptive responses and microglial p38 mitogen-activated protein kinase phosphorylation in trigeminal nucleus caudalis in mouse orofacial formalin model.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021
    Article
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  19. Review
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73 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Koichi ObataDepartment of Anatomy and Neuroscience, Hyogo College of Medicine, Hyogo 663-8501, Japan.
Hiroki Yamanaka
Kimiko Kobayashi
Yi Dai
Toshiyuki Mizushima
Hirokazu Katsura
Tetsuo Fukuoka
Atsushi Tokunaga
Koichi Noguchi
Hyogo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate whether activation of mitogen-activated protein kinase (MAPK) in damaged and/or undamaged primary afferents participates in neuropathic pain after partial nerve injury, we examined the phosphorylation of extracellular signal-regulated protein kinase (ERK), p38 MAPK, and c-Jun N-terminal kinase (JNK) in the L4 and L5 dorsal root ganglion (DRG) in the L5 spinal nerve ligation (SNL) model. We first confirmed, using activating transcription factor 3 and neuropeptide Y immunoreactivity, that virtually all L4 DRG neurons are spared from axotomy in this model. In the injured L5 DRG, the L5 SNL induced the activation of ERK, p38, and JNK in different populations of DRG neurons. In contrast, in the uninjured L4 DRG, the L5 SNL induced only p38 activation in tyrosine kinase A-expressing small- to medium-diameter neurons. Intrathecal ERK, p38, and JNK inhibitor infusions reversed SNL-induced mechanical allodynia, whereas only p38 inhibitor application attenuated SNL-induced thermal hyperalgesia. Furthermore, the L5 dorsal rhizotomy did not prevent SNL-induced thermal hyperalgesia. We therefore hypothesized that p38 activation in the uninjured L4 DRG might be involved in the development of heat hypersensitivity in the L5 SNL model. In fact, the treatment of the p38 inhibitor and also anti-nerve growth factor reduced SNL-induced upregulation of brain-derived neurotrophic factor and transient receptor potential vanilloid type 1 expression in the L4 DRG. Together, our results demonstrate that the L5 SNL induces differential activation of MAPK in injured and uninjured DRG neurons and, furthermore, that MAPK activation in the primary afferents may participate in generating pain hypersensitivity after partial nerve injury.

Indexed as

AnimalsAnthracenesBrain-Derived Neurotrophic FactorButadienesEnzyme ActivationGanglia, SpinalGene Expression RegulationHot TemperatureHyperalgesiaImidazolesIon ChannelsJNK Mitogen-Activated Protein KinasesLigationLumbar VertebraeMaleMAP Kinase Signaling SystemAnthracenesBrain-Derived Neurotrophic FactorButadienesFR 167653ImidazolesIon ChannelsJNK Mitogen-Activated Protein KinasesMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Nitrilesp38 Mitogen-Activated Protein KinasespyrazolanthronePyrazolesPyridinesSB 203580Trpv1 protein, ratTRPV Cation ChannelsU 0126

Identifiers

PMID15537893
PMCPMC6730193
OpenAlexW2094350954

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.