Evidence map›Paper›PMID 24041961›Full record

ArticlePain2014

Roles of glutamate, substance P, and gastrin-releasing peptide as spinal neurotransmitters of histaminergic and nonhistaminergic itch.

Tasuku Akiyama, Mitsutoshi Tominaga, Kenji Takamori, Mirela Iodi Carstens, E Carstens

Open access · greenAbstract read
In one paragraph

Article in Pain, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
12.6field-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

46 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Critical Players and Therapeutic Targets in Chronic Itch.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. A neuropeptide code for itch.Nature reviews. Neuroscience · 2021
    Review
  10. Estrogens influence female itch sensitivity via the spinal gastrin-releasing peptide receptor neurons.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Article
  12. TRPV1 in Pain and Itch.Advances in experimental medicine and biology · 2021
    Article
  13. Low-Threshold Mechanosensitive VGLUT3-Lineage Sensory Neurons Mediate Spinal Inhibition of Itch by Touch.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  14. Physiology and Pathophysiology of Itch.Physiological reviews · 2020
    Review
  15. Article
  16. The Challenge of Basic Itch Research.Acta dermato-venereologica · 2020
    Review
  17. Article
  18. Article
  19. Conopeptides promote itch through human itch receptor hMgprX1.Toxicon : official journal of the International Society on Toxinology · 2018
    Article
  20. 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

5 authors at 2 institutions in 2 countries.

Tasuku AkiyamaDepartment of Neurobiology, Physiology & Behavior, University of California, Davis, CA, USA Institute for Environmental and Gender Specific Medicine, Juntendo University Graduate School of Medicine, Urayasu, Chiba 279-0021, Japan.
Mitsutoshi Tominaga
Kenji Takamori
Mirela Iodi Carstens
E Carstens
University of California, Davis · USJuntendo University · JP

Funding

Spinal mechanisms of itchR01AR057194 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARSTENS, EARL E · 2009 to 2019
$3.4M
Trigeminal Mechanisms of Oral IrritationR01DE013685 · NIDCR · UNIVERSITY OF CALIFORNIA DAVIS · PI CARSTENS, EARL E · 2001 to 2009
$2.1M
Warmth enhancement of itch via TRPV4R00AR063228 · NIAMS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI AKIYAMA, TASUKU · 2014 to 2016
$705k
Rodent model to distinguish between facial itch and painR21DE021183 · NIDCR · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CARSTENS, EARL E · 2010 to 2011
$343k
Warmth enhancement of itch via TRPV4K99AR063228 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI AKIYAMA, TASUKU · 2013 to 2014
$176k
NIAMS NIH HHS AR057194NIAMS NIH HHS AR063228NIAMS NIH HHS K99 AR063228NIAMS NIH HHS R00 AR063228NIAMS NIH HHS R01 AR057194NIDCR NIH HHS DE013685NIDCR NIH HHS R01 DE013685NIDCR NIH HHS R21 DE021183
6 · The paper itself

Abstract

We investigated roles for substance P (SP), gastrin-releasing peptide (GRP), and glutamate in the spinal neurotransmission of histamine-dependent and -independent itch. In anesthetized mice, responses of single superficial dorsal horn neurons to intradermal (i.d.) injection of chloroquine were partially reduced by spinal application of the α-amino-3-hydroxy-5-methyl-4-isoxazole proprionate acid (AMPA)/kainate antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX). Co-application of CNQX plus a neurokinin-1 (NK-1) antagonist produced stronger inhibition, while co-application of CNQX, NK-1, and GRP receptor (GRPR) antagonists completely inhibited firing. Nociceptive-specific and wide dynamic range-type neurons exhibited differential suppression by CNQX plus either the GRPR or NK-1 antagonist, respectively. Neuronal responses elicited by i.d. histamine were abolished by CNQX alone. In behavioral studies, individual intrathecal administration of a GRPR, NK-1, or AMPA antagonist each significantly attenuated chloroquine-evoked scratching behavior. Co-administration of the NK-1 and AMPA antagonists was more effective, and administration of all 3 antagonists abolished scratching. Intrathecal CNQX alone prevented histamine-evoked scratching behavior. We additionally employed a double-label strategy to investigate molecular markers of pruritogen-sensitive dorsal root ganglion (DRG) cells. DRG cells responsive to histamine and/or chloroquine, identified by calcium imaging, were then processed for co-expression of SP, GRP, or vesicular glutamate transporter type 2 (VGLUT2) immunofluorescence. Subpopulations of chloroquine- and/or histamine-sensitive DRG cells were immunopositive for SP and/or GRP, with >80% immunopositive for VGLUT2. These results indicate that SP, GRP, and glutamate each partially contribute to histamine-independent itch. Histamine-evoked itch is mediated primarily by glutamate, with GRP playing a lesser role. Co-application of NK-1, GRP, and AMPA receptor antagonists may prove beneficial in treating chronic itch.

Indexed as

6-Cyano-7-nitroquinoxaline-2,3-dioneAction PotentialsAnimalsAntirheumatic AgentsBombesinChloroquineDrug CombinationsExcitatory Amino Acid AntagonistsGanglia, SpinalGastrin-Releasing PeptideGlutamic AcidMaleMiceMice, Inbred C57BLNeurokinin-1 Receptor AntagonistsNeurons3-((3,5-bis(trifluoromethyl)phenyl)methyloxy)-2-phenylpiperidine6-Cyano-7-nitroquinoxaline-2,3-dioneAntirheumatic AgentsBombesinbombesin (6-14), Tpi(6)-Leu(13)-psi(CH2NH)-Leu(14)-ChloroquineDrug CombinationsExcitatory Amino Acid AntagonistsGastrin-Releasing PeptideGlutamic AcidNeurokinin-1 Receptor AntagonistsPeptide FragmentsPiperidinesSubstance PVesicular Glutamate Transport Protein 2Gastrin-releasing peptideGlutamateHistamineItchScratchingSubstance P

Identifiers

PMID24041961
PMCPMC3947363
OpenAlexW2135906456

What OpenQuestion holds

Textmetadata
LicenceTDM
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.