Evidence map›Paper›PMID 11331395›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Differential contribution of substance P and neurokinin A to spinal cord neurokinin-1 receptor signaling in the rat.

J A Trafton, C Abbadie, A I Basbaum

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 60 citations in OpenAlex.

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  17. Review
  18. Inhibition by spinal mu- and delta-opioid agonists of afferent-evoked substance P release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  19. Article
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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

3 authors at 2 institutions in 1 country.

J A TraftonDepartments of Anatomy and Physiology and W. M. Keck Foundation for Integrative Neuroscience, University of California San Francisco, San Francisco, California 94143.
C Abbadie
A I Basbaum
University of California, San Francisco · USW. M. Keck Foundation · US

Funding

TRIGEMINAL PAIN--MECHANISMS AND CONTROLP01DE008973 · NIDCR · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI JULIUS, DAVID J · 1990 to 2005
$6.2M
Painful Diabetic NeuropathyP50NS021445 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI FIELDS, HOWARD L · 1996 to 2004
$6.0M
BRAINSTEM CONTROL OF PAIN TRANSMISSIONR01NS014627 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BASBAUM, ALLAN I. · 1985 to 2016
$3.9M
Brainstem control of pain transmissionR37NS014627 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BASBAUM, ALLAN I. · 2008 to 2014
$3.6M
Therapeutic/Mechanistic Role of Ape1 in Germ Cell TumorsR01CA094025 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KELLEY, MARK R. · 2003 to 2007
$1.1M
TRIGEMINAL PAIN--MECHANISMS AND CONTROLP50DE008973 · NIDCR · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI LEVINE, JON DAVID · 1991 to 1994
–
NEUROCHEMISTRY OF PAIN MODULATIONP01NS021445 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI RALSTON, HENRY J · 1985 to 1995
–
NCI NIH HHS R01 CA094025NIDCR NIH HHS DE 08973NIDCR NIH HHS P01 DE008973NINDS NIH HHS NS 14627NINDS NIH HHS NS 21445NINDS NIH HHS P50 NS021445NINDS NIH HHS R01 NS014627NINDS NIH HHS R37 NS014627
6 · The paper itself

Abstract

Although the tachykinins substance P (SP) and neurokinin A (NKA) are coreleased from primary afferent nociceptors and act via neurokinin (NK) receptors, their differential effects in vivo are not known. Despite pharmacological evidence that NKA preferentially binds NK-2 receptors, this receptor is not found in spinal cord neurons. Thus, in the present studies, we compared the extent to which SP and NKA contribute to spinal nociceptive processing via the NK-1 receptor. We found that SP and NKA induce NK-1 receptor internalization with identical dose dependence and induce increases in intracellular calcium at the same concentrations, suggesting that SP and NKA equally activate the NK-1 receptor. We found, however, that the selective NK-1 receptor antagonist GR 205171 blocked NKA but not SP-induced NK-1 receptor internalization in the rat spinal cord in vivo and in embryonic day 19 rat spinal neurons in vitro. Using this selectivity of GR 205171 for NKA-induced NK-1 receptor activation, we examined the relative contribution of SP and NKA to noxious stimulus-induced activation of spinal NK-1 receptors. We estimate that NKA contributes to at least 50% of the NK-1 receptor activation in lamina I. Under inflammatory conditions, all noxious stimulus-induced NK-1 receptor internalization in deep dorsal horn neurons was blocked by GR 205171, suggesting that it is entirely NKA-mediated. Substance P-mediated NK-1 receptor internalization was focused at the site of termination of stimulated nociceptors but NKA also activated NK-1 receptors at more distant sites. We conclude that NKA not only targets the NK-1 receptor but may be a predominant pronociceptive primary afferent neurotransmitter.

Indexed as

AnimalsCalciumCells, CulturedDose-Response Relationship, DrugIntracellular FluidMaleNeurokinin-1 Receptor AntagonistsNeurokinin ANeuronsPain MeasurementPiperidinesRatsRats, Sprague-DawleyReceptors, Neurokinin-1Signal TransductionSpinal CordCalciumNeurokinin-1 Receptor AntagonistsNeurokinin APiperidinesReceptors, Neurokinin-1Substance PTetrazolesvofopitant

Identifiers

PMID11331395
PMCPMC6762493
OpenAlexW1792780222

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.