Evidence map›Paper›PMID 20888891›Full record

ArticleNeuroscience2010

Spinal cord mechanisms mediating behavioral hyperalgesia induced by neurokinin-1 tachykinin receptor activation in the rostral ventromedial medulla.

S C Lagraize, W Guo, K Yang, F Wei, K Ren, R Dubner

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

32 citing papers in PubMed, 53 citations in OpenAlex.

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  17. Descending pain modulation and chronification of pain.Current opinion in supportive and palliative care · 2014
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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

6 authors at 1 institution in 1 country.

S C LagraizeUniversity of Maryland Dental School, Department of Neural and Pain, Sciences, Program in Neuroscience, 650 W. Baltimore Street, 8-South, Baltimore, MD 21201, USA. slagraize@umaryland.edu
W Guo
K Yang
F Wei
K Ren
R Dubner
University of Maryland, Baltimore · US

Funding

TRAINING IN OROFACIAL BIOLOGY AND NEUROSCIENCET32DE007309 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI GORDON, SHARON M. · 1997 to 2012
$6.8M
Central glia/cytokines and descending facilitation in orofacial neuropathic painR01DE018573 · NIDCR · UNIVERSITY OF MARYLAND BALTIMORE · PI WEI, FENG · 2007 to 2011
$1.8M
Glial-cytokine-neuronal interactions in the mechanisms of persistent painR01NS060735 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI REN, KE · 2008 to 2012
$1.6M
Descending modulation of behavioral hyperalgesia after injuryR01NS059028 · NINDS · UNIVERSITY OF MARYLAND BALTIMORE · PI DUBNER, RONALD · 2007 to 2011
$1.6M
NIDCR NIH HHS DE018573NIDCR NIH HHS R01 DE018573NIDCR NIH HHS T32 DE007309NIDCR NIH HHS T32DE007309NINDS NIH HHS NS059028NINDS NIH HHS NS060735NINDS NIH HHS R01 NS059028NINDS NIH HHS R01 NS060735
6 · The paper itself

Abstract

Hyperalgesia in animal injury models is linked to activation of descending raphespinal modulatory circuits originating in the rostral ventromedial medulla (RVM). A neurokinin-1 (NK-1) receptor antagonist microinjected into the RVM before or after inflammation produced by complete Freund's adjuvant (CFA) resulted in an attenuation of thermal hyperalgesia. A transient (acute) or a continuous infusion of Substance P (SP) microinjected into the RVM of non-inflamed animals led to similar pain hypersensitivity. Intrathecal pretreatment or post-treatment of a 5-HT3 receptor antagonist (Y-25130 or ondansetron) blocked the SP-induced hyperalgesia. The SP-induced hyperalgesia was both GABA(A) and NMDA receptor-dependent after pre- and post-treatment with selective antagonists at the spinal level. A microinjection of SP into the RVM also led to increased NMDA NR1 receptor subunit phosphorylation in spinal cord tissue. The GABA(A) receptor-mediated hyperalgesia involved a shift in the anionic gradient in dorsal horn nociceptive neurons and an increase in phosphorylated NKCC1 protein (isoform of the Na-K-Cl cotransporter). Following a low dose of SP infused into the RVM, intrathecal muscimol (GABA(A) agonist) increased SP-induced thermal hyperalgesia, phosphorylated NKCC1 protein expression, and NMDA NR1 subunit phosphorylation in the spinal cord. The thermal hyperalgesia was blocked by intrathecal gabazine, the GABA(A) receptor antagonist, and MK-801, the NMDA receptor channel blocker. These findings indicate that NK-1 receptors in the RVM are involved in SP-induced thermal hyperalgesia, this hyperalgesia is 5-HT3-receptor dependent at the spinal level, and involves the functional interaction of spinal GABA(A) and NMDA receptors.

Indexed as

AnimalsBehavior, AnimalBridged Bicyclo Compounds, HeterocyclicDisease Models, AnimalDizocilpine MaleateDose-Response Relationship, DrugDrug Administration ScheduleDrug InteractionsExcitatory Amino Acid AntagonistsFreund's AdjuvantGABA AgentsHyperalgesiaInflammationIn Vitro TechniquesMaleMedulla Oblongata3,5-bis(trifluoromethyl)benzyl N-acetyltryptophanazasetronBridged Bicyclo Compounds, HeterocyclicDizocilpine MaleateExcitatory Amino Acid AntagonistsFreund's AdjuvantGABA AgentsgabazineMuscimolOndansetronOxazinesPyridazinesReceptors, Neurokinin-1Serotonin AntagonistsSubstance PTryptophan

Identifiers

PMID20888891
PMCPMC3006078
OpenAlexW2132549675

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.