Evidence map›Paper›PMID 19494188›Full record

ArticleJournal of neurophysiology2009

Substance P enhances excitatory synaptic transmission on spinally projecting neurons in the rostral ventromedial medulla after inflammatory injury.

Liang Zhang, Donna L Hammond

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Hypofunction of glutamatergic neurotransmission in the periaqueductal gray contributes to nerve-injury-induced neuropathic pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

2 authors at 1 institution in 1 country.

Liang ZhangDepartment of Anesthesia, The University of Iowa, Iowa City, Iowa 52242, USA. Academic_neuroscience@hotmail.com
Donna L Hammond
University of Iowa · US

Funding

OPIOID MECHANISMS OF ANALGESIAR01DA006736 · NIDA · UNIVERSITY OF IOWA · PI HAMMOND, DONNA L · 1991 to 2013
$3.7M
Role of Medullary Substance P in Acute and Persistent NociceptionR01DA023576 · NIDA · UNIVERSITY OF IOWA · PI HAMMOND, DONNA L · 2008 to 2012
$2.6M
A dose ranging study of modafinil for methamphetamine dependenceR01DA023567 · NIDA · CALIFORNIA PACIFIC MED CTR RES INSTITUTE · PI GALLOWAY, GANTT P · 2008 to 2012
$1.5M
NIDA NIH HHS R01 DA-023567NIDA NIH HHS R01 DA023576NIDA NIH HHS R01 DA-06736
6 · The paper itself

Abstract

It has been proposed, but not directly tested, that persistent inflammatory nociception enhances excitatory glutamatergic inputs to neurons in the rostral ventromedial medulla (RVM), altering the activity and function of these neurons. This study used whole cell patch-clamp methods to record evoked excitatory postsynaptic currents (eEPSCs) in spinally projecting RVM neurons from rats injected with saline or complete Freund's adjuvant (CFA) 3-4 days earlier and to examine the role of substance P (SP) in modulating excitatory synaptic transmission. Input-output relationships demonstrated that CFA treatment facilitated fast excitatory glutamatergic inputs to type 1 and type 2 nonserotonergic spinally projecting RVM neurons, but not to type 3 neurons. The facilitation in type 1 and 2 neurons was dependent on neurokinin-1 (NK1) and N-methyl-d-aspartate (NMDA) receptors and prevented by the PKC inhibitor GF109203X. In a subset of neurons from naïve rats, SP mimicked the effects of CFA and increased the potency and efficacy of glutamatergic synaptic transmission. The facilitation was prevented by 10 microM GF109203X, but not by 10 microM KN93, a CaMKII inhibitor. SP (0.3-3 microM) by itself produced concentration-dependent inward currents in most nonserotonergic, but not serotonergic neurons. The present study is the first demonstration, at the cellular level, that persistent inflammatory nociception leads to a sustained facilitation of fast excitatory glutamatergic inputs to RVM neurons by an NK1 and NMDA receptor-dependent mechanism that involves PKC. Further, it demonstrates that the facilitation is restricted to specific populations of RVM neurons that by inference may be pain facilitatory neurons.

Indexed as

AnimalsBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein Kinase Type 2Enzyme InhibitorsExcitatory Postsynaptic PotentialsGlutamic AcidIndolesInflammationIn Vitro TechniquesMaleMaleimidesMedulla OblongataNeural PathwaysNeuronsNeurotransmitter AgentsBenzenesulfonamidesBenzylaminesbisindolylmaleimide ICalcium-Calmodulin-Dependent Protein Kinase Type 2Enzyme InhibitorsGlutamic AcidIndolesKN 93MaleimidesNeurotransmitter AgentsProtein Kinase CReceptors, Neurokinin-1Receptors, N-Methyl-D-AspartateSerotoninSubstance PSulfonamides

Identifiers

PMID19494188
PMCPMC2724368
OpenAlexW2144712949

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.