Evidence map›Paper›PMID 23689673›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013

Dissociable effects of kappa-opioid receptor activation on impulsive phenotypes in wistar rats.

Brendan M Walker, Jessica L Kissler

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 19% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Release of endogenous dynorphin opioids in the prefrontal cortex disrupts cognition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. κ-Opioid Receptor Activation in Dopamine Neurons Disrupts Behavioral Inhibition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  12. Article
  13. Prefrontal Cortical Kappa Opioid Receptors Attenuate Responses to Amygdala Inputs.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Article
  14. Article
  15. Review
  16. 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.

Brendan M WalkerLaboratory of Alcoholism and Addictions Neuroscience, Department of Psychology, Graduate Program in Neuroscience, Washington State University, Pullman, WA, USA.
Jessica L Kissler
Washington State University · US

Funding

The Role of Kappa-Opioid Receptors in Alcohol Use DisordersR01AA020394 · NIAAA · WASHINGTON STATE UNIVERSITY · PI WALKER, BRENDAN M · 2011 to 2022
$3.8M
NIAAA NIH HHS R01 AA020394NIAAA NIH HHS R01AA020394-01
6 · The paper itself

Abstract

The kappa-opioid receptor (KOR) is the primary target for the endogenous opioid peptide dynorphin (DYN), and KORs reside within brain circuitry underlying the complex integration of information related to different behavioral domains such as motivation, negative affect, and decision-making. Alterations in extended amygdala DYNs and KOR function following chronic alcohol exposure have been shown to mediate escalated alcohol self-administration during acute withdrawal. In addition to excessive alcohol consumption and increased negative affect, other symptoms of alcohol dependence include compromised impulse control. Given that DYN and KOR expressions are dysregulated within prefrontal brain circuitry associated with decision-making and impulse control in alcohol-dependent humans and rodents, and have been shown to modify multiple neurotransmitter systems associated with impulse-control disorders, we hypothesized that KOR activation could contribute to impulsive phenotypes. To test this hypothesis, separate cohorts of male Wistar rats were trained in one of the two animal models of impulsivity: delay-discounting (DD) or stop-signal reaction time (SSRT) tasks, and once stable responding was observed, received intracerebroventricular (ICV) infusions of the KOR agonist U50,488 (0-50 μg) according to a within-subject dosing regimen. The results demonstrated a dissociable effect of U50,488 on impulsive phenotypes related to intolerance to delay or response inhibition, with selective effects in the SSRT. Furthermore, the pro-impulsive effects of KOR activation were rescued by pretreatment with the KOR antagonist nor-binaltorphimine (nor-BNI). Therefore, KOR activation was shown to induce an impulsive phenotype that was nor-BNI-sensitive. Dysregulation of impulsive behavior by increased DYN/KOR activity could serve to increase vulnerability for the initiation, or perpetuate existing patterns of excessive alcohol abuse and can enhance the probability of relapse in dependent individuals. Furthermore, KOR-mediated impulsivity has implications for numerous neuropsychiatric disorders.

Indexed as

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAnalgesics, Non-NarcoticAnimalsConditioning, OperantDose-Response Relationship, DrugImpulsive BehaviorInfusions, IntraventricularMaleNaltrexoneNarcotic AntagonistsPhenotypeRatsReceptors, Opioid, kappa3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-IsomerAnalgesics, Non-NarcoticNaltrexoneNarcotic AntagonistsnorbinaltorphimineReceptors, Opioid, kappa

Identifiers

PMID23689673
PMCPMC3773679
OpenAlexW1990201261

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.