Evidence map›Paper›PMID 26359313›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2015

Effects of nicotinic acetylcholine receptor agonists in assays of acute pain-stimulated and pain-depressed behaviors in rats.

Kelen C Freitas, F Ivy Carroll, S Stevens Negus

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Spider venom peptides as potential drug candidates due to their anticancer and antinociceptive activities.The journal of venomous animals and toxins including tropical diseases · 2019
    Review
  8. Review
  9. Article
  10. Article
  11. Relief of Pain-Depressed Behavior in Rats by Activation of D1-Like Dopamine Receptors.The Journal of pharmacology and experimental therapeutics · 2017
    Article
  12. 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 2 institutions in 1 country.

Kelen C FreitasDepartment of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia.
F Ivy Carroll
S Stevens Negus
RTI International · USResearch Triangle Park Foundation · US

Funding

Neurobiology and Treatment of PainR01NS070715 · NINDS · VIRGINIA COMMONWEALTH UNIVERSITY · PI NEGUS, SIDNEY S, SELLEY, DANA E · 2009 to 2018
$3.3M
NINDS NIH HHS R01 NS070715
6 · The paper itself

Abstract

Agonists at nicotinic acetylcholine receptors (nAChRs) constitute one drug class being evaluated as candidate analgesics. Previous preclinical studies have implicated α4β2 and α7 nAChRs as potential mediators of the antinociceptive effects of (–)-nicotine hydrogen tartrate (nicotine) and other nAChR agonists; however, these studies have relied exclusively on measures of pain-stimulated behavior, which can be defined as behaviors that increase in frequency, rate, or intensity after presentation of a noxious stimulus. Pain is also associated with depression of many behaviors, and drug effects can differ in assays of pain-stimulated versus pain-depressed behavior. Accordingly, this study compared the effects of nicotine, the selective α4/6β2 agonist 5-(123I)iodo-3-[2(S)-2-azetidinylmethoxy]pyridine (5-I-A-85380), and the selective α7 agonist N-(3R)-1-azabicyclo(2.2.2)oct-3-yl-4-chlorobenzamide in assays of pain-stimulated and pain-depressed behavior in male Sprague-Dawley rats. Intraperitoneal injection of dilute lactic acid served as an acute noxious stimulus to either stimulate a stretching response or depress the operant responding, which is maintained by electrical brain stimulation in an intracranial self-stimulation (ICSS) procedure. Nicotine produced a dose-dependent, time-dependent, and mecamylamine-reversible blockade of both acid-stimulated stretching and acid-induced depression of ICSS. 5-I-A-85380 also blocked both acid-stimulated stretching and acid-induced depression of ICSS, whereas N-(3R)-1-azabicyclo(2.2.2)oct-3-yl-4-chlorobenzamide produced no effect in either procedure. Both nicotine and 5-I-A-85380 were ≥10-fold more potent in blocking the acid-induced depression of ICSS than in blocking the acid-induced stimulation of stretching. These results suggest that stimulation of α4β2 and/or α6β2 nAChRs may be especially effective to alleviate the signs of pain-related behavioral depression in rats; however, nonselective behavioral effects may contribute to apparent antinociception.

Indexed as

Acute DiseaseAnalgesicsAnimalsAzetidinesBehavior, AnimalBenzamidesBrainBridged Bicyclo CompoundsConditioning, OperantElectric StimulationMaleNicotineNicotinic AgonistsPainPyridinesRats, Sprague-Dawley2-fluoro-3-(2-azetidinylmethoxy)pyridineAnalgesicsAzetidinesBenzamidesBridged Bicyclo CompoundsNicotineNicotinic AgonistsPNU-282987Pyridines

Identifiers

PMID26359313
PMCPMC4613961
OpenAlexW2167314430

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.