Evidence map›Paper›PMID 26770021›Full record

ArticleMediators of inflammation2015

Peripheral NMDA Receptors Mediate Antidromic Nerve Stimulation-Induced Tactile Hypersensitivity in the Rat.

Jun Ho Jang, Taick Sang Nam, Jaebeom Jun, Se Jung Jung, Dong-Wook Kim, Joong Woo Leem

Open access · goldAbstract read
In one paragraph

Article in Mediators of inflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.4field-weighted citation impact, top 34% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
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

6 authors at 2 institutions in 1 country.

Jun Ho JangDental Research Institute, Seoul National University, Seoul 110-744, Republic of Korea.
Taick Sang NamDepartment of Physiology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea; Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea.
Jaebeom JunDepartment of Physiology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea; Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea.
Se Jung JungDepartment of Physiology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea; Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea.
Dong-Wook KimDepartment of Physiology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea; Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea.
Joong Woo LeemDepartment of Physiology, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea; Brain Research Institute, Yonsei University College of Medicine, Seoul 120-752, Republic of Korea; Graduate Program in Cognitive Science Yonsei University, Seoul 120-752, Republic of Korea.
Yonsei University · KRSeoul National University Dental Hospital · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the role of peripheral NMDA receptors (NMDARs) in antidromic nerve stimulation-induced tactile hypersensitivity outside the skin area innervated by stimulated nerve. Tetanic electrical stimulation (ES) of the decentralized L5 spinal nerve, which induced enlargement of plasma extravasation, resulted in tactile hypersensitivity in the L4 plantar dermatome of the hind-paw. When intraplantar (i.pl.) injection was administered into the L4 dermatome before ES, NMDAR and group-I metabotropic Glu receptor (mGluR) antagonists and group-II mGluR agonist but not AMPA/kainate receptor antagonist prevented ES-induced hypersensitivity. I.pl. injection of PKA or PKC inhibitors also prevented ES-induced hypersensitivity. When the same injections were administered after establishment of ES-induced hypersensitivity, hypersensitivity was partially reduced by NMDAR antagonist only. In naïve animals, i.pl. Glu injection into the L4 dermatome induced tactile hypersensitivity, which was blocked by NMDAR antagonist and PKA and PKC inhibitors. These results suggest that the peripheral release of Glu, induced by antidromic nerve stimulation, leads to the expansion of tactile hypersensitive skin probably via nociceptor sensitization spread due to the diffusion of Glu into the skin near the release site. In addition, intracellular PKA- and PKC-dependent mechanisms mediated mainly by NMDAR activation are involved in Glu-induced nociceptor sensitization and subsequent hypersensitivity.

Indexed as

AnimalsCyclic AMP-Dependent Protein KinasesDizocilpine MaleateElectric StimulationGlutamic AcidHyperalgesiaIsoquinolinesMaleProtein Kinase CQuinoxalinesRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateSulfonamidesTibial Nerve2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxalineCyclic AMP-Dependent Protein KinasesDizocilpine MaleateGlutamic AcidIsoquinolinesN-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamideProtein Kinase CQuinoxalinesReceptors, N-Methyl-D-AspartateSulfonamides

Identifiers

PMID26770021
PMCPMC4681795
OpenAlexW2182228709

What OpenQuestion holds

Textmetadata
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.