Evidence map›Paper›PMID 17267128›Full record

ArticlePain2007

Altered spinal arachidonic acid turnover after peripheral nerve injury regulates regional glutamate concentration and neuropathic pain behaviors in rats.

Backil Sung, Shuxing Wang, Bei Zhou, Grewo Lim, Liling Yang, Qing Zeng, Jeong-Ae Lim, Jing Dong Wang, Jing X Kang, Jianren Mao

Open access · greenAbstract read
In one paragraph

Article in Pain, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-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

22 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  6. Phospholipase AACS nano · 2020
    Article
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  9. Guanosine and its role in neuropathologies.Purinergic signalling · 2016
    Review
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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

10 authors at 1 institution in 1 country.

Backil SungPain Research Group, Division of Pain Medicine, WACC 324, Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, 15 Parkman Street, Boston, MA 02114, USA.
Shuxing Wang
Bei Zhou
Grewo Lim
Liling Yang
Qing Zeng
Jeong-Ae Lim
Jing Dong Wang
Jing X Kang
Jianren Mao
Massachusetts General Hospital · US

Funding

NEURAL AND MOLECULAR MECHANISMS OF HYPERALGESIAR01DA008835 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI MAO, JIANREN · 1995 to 2005
$1.8M
Glutamate Uptake &the Pathogenesis of Neuropathic PainR01NS045681 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MAO, JIANREN · 2004 to 2007
$1.4M
Neuropathic Pain Modulation by CannabinoidsR01NS042661 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI MAO, JIANREN · 2003 to 2006
$1.3M
NIDA NIH HHS R01 DA008835NINDS NIH HHS R01 NS042661NINDS NIH HHS R01 NS045681NINDS NIH HHS R01 NS42661NINDS NIH HHS R01 NS45681
6 · The paper itself

Abstract

Spinal glutamate transporters (GT) have been implicated in the mechanisms of neuropathic pain; however, how spinal GT uptake activity is regulated remains unclear. Here we show that alteration of spinal arachidonic acid (AA) turnover after peripheral nerve injury regulated regional GT uptake activity and glutamate homeostasis. Chronic constriction nerve injury (CCI) in rats significantly reduced spinal GT uptake activity ((3)H-glutamate uptake) with an associated increase in extracellular AA and glutamate concentration from spinal microdialysates on postoperative day 8. AACOCF3 (a cytosolic phospholipase A2 inhibitor, 30mug) given intrathecally twice a day for postoperative day 1-7 reversed this CCI-induced spinal AA production, prevented the reduced spinal GT uptake activity and increased extracellular glutamate concentration. Conversely, alteration of spinal AA metabolism by diclofenac (a cyclooxygenase 1/2 inhibitor, 200mug) further reduced spinal GT uptake activity and increased extracellular glutamate concentration in CCI rats. GT uptake activity was also attenuated when AA (10 or 100nM) was directly added into spinal samples of naïve rats in an in vitro(3)H-glutamate uptake assay, indicating a direct inhibitory effect of AA on GT uptake activity. Consistent with these findings, AACOCF3 reduced the development of both thermal hyperalgesia and mechanical allodynia, whereas diclofenac exacerbated thermal hyperalgesia, in CCI rats. Thus, spinal AA turnover may serve as a regulator in CCI-induced changes in regional GT uptake activity, glutamate homeostasis, and neuropathic pain behaviors. These data suggest that regulating spinal AA turnover may be a useful approach to improving the clinical management of neuropathic pain.

Indexed as

Behavior, AnimalAdaptation, PhysiologicalAnimalsArachidonic AcidGlutamic AcidHyperalgesiaMaleMetabolic Clearance RateRatsRats, Sprague-DawleySciatic NerveSpinal CordArachidonic AcidGlutamic Acid

Identifiers

PMID17267128
PMCPMC2478515
OpenAlexW2145983425

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.