Evidence map›Paper›PMID 24184981›Full record

ArticleNeuroscience2014

Inflammation enhances Y1 receptor signaling, neuropeptide Y-mediated inhibition of hyperalgesia, and substance P release from primary afferent neurons.

B K Taylor, W Fu, K E Kuphal, C-O Stiller, M K Winter, W Chen, G F Corder, J H Urban, K E McCarson, J C Marvizon

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  5. Spinal neuropeptide Y Y1 receptor-expressing neurons are a pharmacotherapeutic target for the alleviation of neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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 6 institutions in 2 countries.

B K TaylorDepartment of Physiology, School of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, USA. Electronic address: brad.taylor@uky.edu.
W FuDepartment of Physiology, School of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, USA.
K E KuphalDivision of Pharmacology, University of Missouri-Kansas City, Kansas City, MO, USA.
C-O StillerDepartment of Medicine, Division of Clinical Pharmacology, Karolinska Hospital, Karolinska Institutet, Stockholm, Sweden.
M K WinterDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA.
W ChenVeteran Affairs Greater Los Angeles Healthcare System and Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
G F CorderDepartment of Physiology, School of Medicine, University of Kentucky Medical Center, Lexington, KY 40536, USA.
J H UrbanDepartment of Physiology and Biophysics, The Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, IL, USA.
K E McCarsonDepartment of Pharmacology, Toxicology and Therapeutics, University of Kansas Medical Center, Kansas City, KS 66160, USA.
J C MarvizonVeteran Affairs Greater Los Angeles Healthcare System and Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine at the University of California Los Angeles, Los Angeles, CA, USA.
University of Kentucky · USUniversity of California, Los Angeles · USUniversity of Kansas Medical Center · USKarolinska University Hospital · SERosalind Franklin University of Medicine and Science · USUniversity of Missouri–Kansas City · US

Funding

Research Design and Analysis Core (RDAC)P30HD002528 · NICHD · UNIVERSITY OF KANSAS LAWRENCE · PI FOWLER, STEPHEN CLETIUS · 1985 to 2015
$22.1M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
NEUROPEPTIDERGIC INHIBITION OF SPINAL PAIN TRANSMISSIONR01NS045954 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BRADLEY K. TAYLOR · 2002 to 2026
$7.4M
NMDA Receptors in Primary AfferentsR01DA033059 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MARVIZON, JUAN CARLOS GARCIA, MCROBERTS, JAMES A · 2012 to 2016
$1.4M
Neuropeptidergic Inhibition of Spinal Pain TransmissionK02DA019656 · NIDA · UNIVERSITY OF KENTUCKY · PI TAYLOR, BRADLEY K. · 2007 to 2011
$574k
NICHD NIH HHS HD02528NICHD NIH HHS P30 HD002528NIDA NIH HHS K02 DA019656NIDA NIH HHS K02DA19656NIDA NIH HHS R01 DA033059NIDDK NIH HHS P30 DK041301NINDS NIH HHS R01 NS045954NINDS NIH HHS R01NS45954
6 · The paper itself

Abstract

Neuropeptide Y (NPY) is present in the superficial laminae of the dorsal horn and inhibits spinal nociceptive processing, but the mechanisms underlying its anti-hyperalgesic actions are unclear. We hypothesized that NPY acts at neuropeptide Y1 receptors in the dorsal horn to decrease nociception by inhibiting substance P (SP) release, and that these effects are enhanced by inflammation. To evaluate SP release, we used microdialysis and neurokinin 1 receptor (NK1R) internalization in rat. NPY decreased capsaicin-evoked SP-like immunoreactivity in the microdialysate of the dorsal horn. NPY also decreased non-noxious stimulus (paw brush)-evoked NK1R internalization (as well as mechanical hyperalgesia and mechanical and cold allodynia) after intraplantar injection of carrageenan. Similarly, in rat spinal cord slices with dorsal root attached, [Leu(31), Pro(34)]-NPY inhibited dorsal root stimulus-evoked NK1R internalization. In rat dorsal root ganglion neurons, Y1 receptors colocalized extensively with calcitonin gene-related peptide (CGRP). In dorsal horn neurons, Y1 receptors were extensively expressed and this may have masked the detection of terminal co-localization with CGRP or SP. To determine whether the pain inhibitory actions of Y1 receptors are enhanced by inflammation, we administered [Leu(31), Pro(34)]-NPY after intraplantar injection of complete Freund's adjuvant (CFA) in rat. We found that [Leu(31), Pro(34)]-NPY reduced paw clamp-induced NK1R internalization in CFA rats but not uninjured controls. To determine the contribution of increased Y1 receptor-G protein coupling, we measured [(35)S]GTPγS binding simulated by [Leu(31), Pro(34)]-NPY in mouse dorsal horn. CFA inflammation increased the affinity of Y1 receptor G-protein coupling. We conclude that Y1 receptors contribute to the anti-hyperalgesic effects of NPY by mediating the inhibition of SP release, and that Y1 receptor signaling in the dorsal horn is enhanced during inflammatory nociception.

Indexed as

AnimalsFreund's AdjuvantGuanosine 5'-O-(3-Thiotriphosphate)HyperalgesiaInflammationIn Vitro TechniquesMaleNeurons, AfferentNeuropeptide YPain MeasurementPain ThresholdProtein BindingRatsRats, Sprague-DawleyReceptors, Neurokinin-1Receptors, Neuropeptide YFreund's AdjuvantGuanosine 5'-O-(3-Thiotriphosphate)Neuropeptide YReceptors, Neurokinin-1Receptors, Neuropeptide YSubstance PSulfur Isotopes2-[4-(2-hydroxyethyl)piperazin-1-yl]ethanesulfonic acidaCSFanalysis of varianceANOVAartificial cerebrospinal fluidcalcitonin gene-related peptidecapsaicinCFACGRPcomplete Freund’s adjuvantdorsal root ganglionDRGG-proteinHEPESIB4isolectin B4isolectin-B4neurokinin 1 receptorneurokinin-1 receptorneuropeptide YNK1RNPYpainPBSphosphate-buffered salineradioimmunoassayRIASPSP-LISP-like immunoreactivitysubstance P

Identifiers

PMID24184981
PMCPMC4363128
OpenAlexW2064915633

What OpenQuestion holds

Textmetadata
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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.