Evidence map›Paper›PMID 26775017›Full record

ArticleNeurobiology of learning and memory2016

Cognitive control deficits during mecamylamine-precipitated withdrawal in mice: Possible links to frontostriatal BDNF imbalance.

Vinay Parikh, Robert D Cole, Purav J Patel, Rachel L Poole, Thomas J Gould

Abstract read
In one paragraph

Article in Neurobiology of learning and memory, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Cognitive rigidity and BDNF-mediated frontostriatal glutamate neuroadaptations during spontaneous nicotine withdrawal.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Article
  4. Article
  5. Article
  6. Accumbal Adenosine AFrontiers in cellular neuroscience · 2019
    Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. 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

5 authors at 1 institution in 1 country.

Vinay ParikhDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA 19122, United States. Electronic address: vinay.parikh@temple.edu.
Robert D ColeDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA 19122, United States.
Purav J PatelDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA 19122, United States.
Rachel L PooleDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA 19122, United States.
Thomas J GouldDepartment of Psychology and Neuroscience Program, Temple University, Philadelphia, PA 19122, United States.
Temple University · US

Funding

Nicotine Addiction: Learning, Neural &Genetic ProcessR01DA017949 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI GOULD, THOMAS J · 2005 to 2015
$2.7M
Cognitive control and corticostriatal BDNF signaling during nicotine withdrawalR03DA037421 · NIDA · TEMPLE UNIV OF THE COMMONWEALTH · PI PARIKH, VINAY · 2015 to 2016
$155k
NIDA NIH HHS DA 017949NIDA NIH HHS DA 037421NIDA NIH HHS R01 DA017949NIDA NIH HHS R03 DA037421
6 · The paper itself

Abstract

Nicotine is a major psychoactive and addictive component of tobacco. Although cessation of tobacco use produces various somatic and affective symptoms, withdrawal-related cognitive deficits are considered to be a critical symptom that predict relapse. Therefore, delineating the cognitive mechanisms of nicotine withdrawal may likely provide gainful insights into the neurobiology of nicotine addiction. The present study was designed to examine the effects of nicotine withdrawal induced by mecamylamine, a non-specific nicotinic receptor (nAChR) antagonist, on cognitive control processes in mice using an operant strategy switching task. Brain-derived neurotrophic factor (BDNF) modulates synaptic transmission in frontostriatal circuits, and these circuits are critical for executive functions. Thus, we examined the effects of mecamylamine-precipitated nicotine withdrawal on prefrontal and striatal BDNF protein expression. Mice undergoing precipitated nicotine withdrawal required more trials to attain strategy switching criterion as compared to the controls. Error analysis indicated that impaired performance in these animals was mostly related to their inability to execute the new strategy. The striatal/prefrontal BDNF ratios robustly increased following precipitated nicotine withdrawal. Moreover, higher BDNF ratios were associated with longer task acquisition. Collectively, our findings illustrate that mecamylamine-induced nicotine withdrawal disrupts cognitive control processes and that these changes are possibly linked to perturbations in frontostriatal BDNF signaling.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCognitionCorpus StriatumExecutive FunctionMaleMecamylamineMiceMice, Inbred C57BLNicotineNicotinic AgonistsNicotinic AntagonistsPrefrontal CortexSubstance Withdrawal SyndromeBrain-Derived Neurotrophic FactorMecamylamineNicotineNicotinic AgonistsNicotinic AntagonistsAddictionBDNFCognitive flexibilityMiceNicotine withdrawal

Identifiers

PMID26775017
PMCPMC4744530
OpenAlexW2233624797

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.