Evidence map›Paper›PMID 25281224›Full record

ArticlePsychopharmacology2015

Contributions of β2 subunit-containing nAChRs to chronic nicotine-induced alterations in cognitive flexibility in mice.

Robert D Cole, Rachel L Poole, Dawn M Guzman, Thomas J Gould, Vinay Parikh

Abstract read
In one paragraph

Article in Psychopharmacology, 2015. 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
–field-weighted citation impact
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.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Rodent models for nicotine withdrawal.Journal of psychopharmacology (Oxford, England) · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Neuregulin 3 Signaling Mediates Nicotine-Dependent Synaptic Plasticity in the Orbitofrontal Cortex and Cognition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  11. Article
  12. Cognitive Effects of Nicotine: Recent Progress.Current neuropharmacology · 2018
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

5 authors.

Robert D ColeDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA, 19122, USA.
Rachel L Poole
Dawn M Guzman
Thomas J Gould
Vinay Parikh

Funding

Neuroimaging Abstinence and Medication ResponseP50CA143187 · NCI · UNIVERSITY OF PENNSYLVANIA · PI AUDRAIN-MCGOVERN, JANET E · 2009 to 2013
$8.6M
Temple University Minority Access to Research Careers (MARC) programT34GM087239 · NIGMS · TEMPLE UNIV OF THE COMMONWEALTH · PI TANAKA, JACQUELINE C · 2009 to 2018
$5.2M
Nicotine Addiction: Learning, Neural &Genetic ProcessR01DA017949 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI GOULD, THOMAS J · 2005 to 2015
$2.7M
NCI NIH HHS CA 143187NCI NIH HHS P50 CA143187NIDA NIH HHS DA 017949NIDA NIH HHS R01 DA017949NIGMS NIH HHS 5T34 GM087239NIGMS NIH HHS T34 GM087239
6 · The paper itself

Abstract

rationaleDeficits in executive functions underlie compulsive drug use, and understanding how nicotine influences these cognitive processes may provide important information on neurobiological substrates of nicotine addiction. Accumulating evidence suggests that β2 subunit-containing nicotinic receptors (nAChRs) are involved in the reinforcing process of nicotine addiction. Whether these nAChRs also contributes to the detrimental effects of chronic nicotine on flexible decision-making is not known.

objectivesIn the present study, the effects of chronic nicotine were assessed in mice with partial or complete deletion of the β2 subunit-containing nAChR gene (β2+/- or β2-/-) performing an operant cognitive flexibility task.

resultsVisual discrimination learning was not affected in saline-treated β2 nAChR mutants as compared to the wild-type (β2+/+) mice; yet, chronic nicotine facilitated acquisition of visual discrimination in all genotypes. The acquisition of new egocentric response strategy set-shifting remained similar in all genotypes, and there was no effect of treatment. Chronic nicotine treatment impaired reversal learning in β2+/+ mice by increasing response perseveration to the previously rewarded stimulus. Moreover, the acquisition of inverted stimulus-reward contingencies did not differ between β2+/+ and β2-/- mice exposed to chronic nicotine. Interestingly, nicotine-induced reversal learning deficits were not observed in β2+/- mice.

conclusionsCollectively, these findings suggest that β2 subunit-containing nAChRs are not critical for visual discrimination learning and extra dimensional rule shift. However, sustained activation of these nAChRs with nicotine may interfere with inhibitory control processes influencing affective shifts in stimulus-reward contingencies.

Indexed as

AnimalsCognitionConditioning, OperantDiscrimination LearningDrug Administration ScheduleMaleMiceMice, Inbred C57BLMice, KnockoutNicotinePhotic StimulationProtein SubunitsReceptors, NicotinicReversal LearningNicotineProtein SubunitsReceptors, Nicotinic

Identifiers

PMID25281224
PMCPMC4361240

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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.