Evidence map›Paper›PMID 19631644›Full record

ArticleExperimental neurology2009

Neurokinins inhibit low threshold inactivating K+ currents in capsaicin responsive DRG neurons.

Adrian Sculptoreanu, Debra E Artim, William C de Groat

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 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
1.2field-weighted citation impact, top 22% 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, 29 citations in OpenAlex.

  1. Article
  2. Recent Developments in On-Demand Voiding Therapies.The Journal of pharmacology and experimental therapeutics · 2024
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. A-Type KFrontiers in molecular neuroscience · 2018
    Review
  8. Action Potential Broadening in Capsaicin-Sensitive DRG Neurons from Frequency-Dependent Reduction of Kv3 Current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  9. Review
  10. Article
  11. Pharmacodynamic evaluation of LysNaunyn-Schmiedeberg's archives of pharmacology · 2017
    Article
  12. Article
  13. Neural control of the lower urinary tract.Comprehensive Physiology · 2015
    Review
  14. Article
  15. Article
  16. Common theme for drugs effective in overactive bladder treatment: inhibition of afferent signaling from the bladder.International journal of urology : official journal of the Japanese Urological Association · 2013
    Review
  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

3 authors at 1 institution in 1 country.

Adrian SculptoreanuDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, PA, USA. ads5@pitt.edu
Debra E Artim
William C de Groat
University of Pittsburgh · US

Funding

AFFERENT MECHANISMS UNDERLYING BLADDER PAINR37DK049430 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI DEGROAT, WILLIAM C · 2000 to 2009
$3.0M
NIDDK NIH HHS R37 DK049430PHS HHS NIDDK 45430
6 · The paper itself

Abstract

Neurokinins (NK) released from terminals of dorsal root ganglion (DRG) neurons may control firing of these neurons by an autofeedback mechanism. In this study we used patch clamp recording techniques to determine if NKs alter excitability of rat L4-S3 DRG neurons by modulating K(+) currents. In capsaicin (CAPS)-responsive phasic neurons substance P (SP) lowered action potential (AP) threshold and increased the number of APs elicited by depolarizing current pulses. SP and a selective NK(2) agonist, [betaAla(8)]-neurokinin A (4-10) also inhibited low threshold inactivating K(+) currents isolated by blocking non-inactivating currents with a combination of high TEA, (-) verapamil and nifedipine. Currents recorded under these conditions were heteropodatoxin-sensitive (Kv4 blocker) and alpha-dendrotoxin-insensitive (Kv1.1 and Kv1.2 blocker). SP and NKA elicited a >10 mV positive shift of the voltage dependence of activation of the low threshold currents. This effect was absent in CAPS-unresponsive neurons. The effect of SP or NKA on K(+) currents in CAPS-responsive phasic neurons was fully reversed by an NK(2) receptor antagonist (MEN10376) but only partially reversed by a PKC inhibitor (bisindolylmaleimide). An NK(1) selective agonist ([Sar(9), Met(11)]-substance P) or direct activation of PKC with phorbol 12,13-dibutyrate, did not change firing in CAPS-responsive neurons, but did inhibit various types of K(+) currents that activated over a wide range of voltages. These data suggest that the excitability of CAPS-responsive phasic afferent neurons is increased by activation of NK(2) receptors and that this is due in part to inhibition and a positive voltage shift in the activation of heteropodatoxin-sensitive Kv4 channels.

Indexed as

Alkanesulfonic AcidsAnimalsBiophysicsCapsaicinCyclohexylaminesDose-Response Relationship, DrugDrug InteractionsElectric StimulationGanglia, SpinalMaleMembrane PotentialsNeural InhibitionNeuronsPatch-Clamp TechniquesPotassium Channel BlockersPotassium Channels3-(cyclohexylamino)-1-propanesulfonic acidAlkanesulfonic AcidsCapsaicinCyclohexylaminesPotassium Channel BlockersPotassium ChannelsSensory System AgentsSubstance PTachykinins

Identifiers

PMID19631644
PMCPMC2775709
OpenAlexW2010798080

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.