Evidence map›Paper›PMID 26041925›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Persistent Nociception Triggered by Nerve Growth Factor (NGF) Is Mediated by TRPV1 and Oxidative Mechanisms.

Michael A Eskander, Shivani Ruparel, Dustin P Green, Paul B Chen, Elaine D Por, Nathaniel A Jeske, Xiaoli Gao, Eric R Flores, Kenneth M Hargreaves

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 1 pooled it
8.3field-weighted citation impact, top 2% 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

68 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

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8 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 4 institutions in 3 countries.

Michael A EskanderDepartment of Pharmacology.
Shivani RuparelDepartment of Endodontics.
Dustin P GreenDepartment of Physiology.
Paul B ChenDepartment of Endodontics.
Elaine D PorDepartment of Pharmacology.
Nathaniel A JeskeDepartment of Pharmacology, Department of Physiology, Department of Oral and Maxillofacial Surgery, and.
Xiaoli GaoDepartment of Biochemistry, University of Texas Health Science Center at San Antonio, San Antonio, Texas 78229.
Eric R FloresDepartment of Pharmacology.
Kenneth M HargreavesDepartment of Pharmacology, Department of Endodontics, Department of Physiology, Hargreaves@UTHSCSA.edu.ORCID http://orcid.org/0000-0002-1076-4931
Institute of Pharmacology · CZAmerican Association of Endodontists · USCzech Academy of Sciences, Institute of Physiology · CZThe University of Texas Health Science Center at San Antonio · US

Funding

Institute for Integration of Medicine & Science: A Partnership to Improve HealthUL1TR001120 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CLARK, ROBERT A, HARGREAVES, KENNETH M · 2013 to 2017
$16.5M
Institutional Research Training GrantT32DE014318 · NIDCR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Kenneth M Hargreaves · 2002 to 2026
$12.1M
Role of Oxidized Linoleic Acid Metabolites in PainR01NS072890 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HARGREAVES, KENNETH M · 2010 to 2014
$1.8M
Scaffolding the Transition to Chronic PainR01NS082746 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI JESKE, NATHANIEL AARON · 2013 to 2017
$1.7M
Evaluation of Endogenous TRP Agonists in Human BurnsR01GM106075 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI HARGREAVES, KENNETH M · 2014 to 2017
$1.2M
South Texas Advanced Research Training: Undergraduate Program (START-UP)R25NS080684 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FRAZER, ALAN, MORILAK, DAVID A · 2012 to 2014
$741k
Triple Quadrupole Mass Spectrometer for Metabolomics AnalysisS10RR031586 · NCRR · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI WEINTRAUB, SUSAN T · 2011 to 2011
$446k
The Role of Oxidized Linoleic Acid Metabolites in NGF Induced Persistent PainF31NS083358 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ESKANDER, MICHAEL ANDREW · 2013 to 2014
$54k
NCATS NIH HHS UL1 TR001120NCRR NIH HHS 1S10RR031586-0NCRR NIH HHS S10 RR031586NIDCR NIH HHS T32 DE014318NIGMS NIH HHS R01 GM106075NIGMS NIH HHS R01GM106075NINDS NIH HHS F31 NS083358NINDS NIH HHS F31NS083358NINDS NIH HHS R01 NS072890NINDS NIH HHS R01NS072890NINDS NIH HHS R01 NS082746NINDS NIH HHS R01NS082746NINDS NIH HHS R25 NS080684
6 · The paper itself

Abstract

Nerve growth factor (NGF) is elevated in certain chronic pain conditions and is a sufficient stimulus to cause lasting pain in humans, but the actual mechanisms underlying the persistent effects of NGF remain incompletely understood. We developed a rat model of NGF-induced persistent thermal hyperalgesia and mechanical allodynia to determine the role of transient receptor potential vanilloid 1 (TRPV1) and oxidative mechanisms in the persistent effects of NGF. Persistent thermal hypersensitivity and mechanical allodynia require de novo protein translation and are mediated by TRPV1 and oxidative mechanisms. By comparing effects after systemic (subcutaneous), spinal (intrathecal) or hindpaw (intraplantar) injections of test compounds, we determined that TRPV1 and oxidation mediate persistent thermal hypersensitivity via peripheral and spinal sites of action and mechanical allodynia via only a spinal site of action. Therefore, NGF-evoked thermal and mechanical allodynia are mediated by spatially distinct mechanisms. NGF treatment evoked sustained increases in peripheral and central TRPV1 activity, as demonstrated by increased capsaicin-evoked nocifensive responses, increased calcitonin gene-related peptide release from hindpaw skin biopsies, and increased capsaicin-evoked inward current and membrane expression of TRPV1 protein in dorsal root ganglia neurons. Finally, we showed that NGF treatment increased concentrations of linoleic and arachidonic-acid-derived oxidized TRPV1 agonists in spinal cord and skin biopsies. Furthermore, increases in oxidized TRPV1-active lipids were reduced by peripheral and spinal injections of compounds that completely blocked persistent nociception. Collectively, these data indicate that NGF evokes a persistent nociceptive state mediated by increased TRPV1 activity and oxidative mechanisms, including increased production of oxidized lipid TRPV1 agonists.

Indexed as

Action PotentialsAnimalsCalcitonin Gene-Related PeptideCapsaicinCells, CulturedCycloheximideEnzyme-Linked Immunosorbent AssayGanglia, SpinalHyperalgesiaMaleNerve Growth FactorNociceptionOxidative StressPain MeasurementProtein Synthesis InhibitorsRatsCalcitonin Gene-Related PeptideCapsaicinCycloheximideNerve Growth FactorProtein Synthesis InhibitorsSensory System AgentsTrpv1 protein, ratTRPV Cation Channelsallodyniaarachidonic acidhyperalgesialinoleic acidnerve growth factorTRPV1

Identifiers

PMID26041925
PMCPMC4452557
OpenAlexW1536951294

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.