Evidence map›Paper›PMID 29100991›Full record

ArticlePharmacology, biochemistry, and behavior2017

Cue-induced reinstatement of alcohol-seeking behavior is associated with increased CaMKII T286 phosphorylation in the reward pathway of mice.

Michael C Salling, Christopher J Hodge, Kelly E Psilos, Vallari R Eastman, Sara P Faccidomo, Clyde W Hodge

Abstract read
In one paragraph

Article in Pharmacology, biochemistry, and behavior, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed.

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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

6 authors.

Michael C SallingCurriculum in Neurobiology, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States.
Christopher J HodgeBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States.
Kelly E PsilosBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States.
Vallari R EastmanBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States.
Sara P FaccidomoBowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States.
Clyde W HodgeDepartment of Psychiatry, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States; Department of Pharmacology, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States; Bowles Center for Alcohol Studies, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States; Curriculum in Neurobiology, University of North Carolina at Chapel Hill, Thurston-Bowles Building; CB #7178, Chapel Hill, NC 27599, United States. Electronic address: chodge@med.unc.edu.

Funding

UNC ARC Information/Dissemination CoreP60AA011605 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Thomas L. Kash · 2003 to 2026
$46.3M
MOLECULAR AND CELLULAR PATHOGENESIS IN ALCOHOLISMP50AA011605 · NIAAA · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI CREWS, FULTON T · 1998 to 2002
$4.9M
Molecular Mechanisms of Ethanol Reinforcement R37AA014983 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HODGE, CLYDE W · 2013 to 2020
$2.7M
NIAAA NIH HHS P50 AA011605NIAAA NIH HHS P60 AA011605NIAAA NIH HHS R37 AA014983
6 · The paper itself

Abstract

Cue-induced reinstatement of alcohol-seeking is a hallmark behavioral pathology of addiction. Evidence suggests that reinstatement (e.g., relapse), may be regulated by cell signaling systems that underlie neuroplasticity. A variety of plasticity events require activation of calcium calmodulin-dependent protein kinase II (CaMKII) in components of the reward pathway, such as the nucleus accumbens and amygdala. We sought to determine if cue-induced reinstatement of alcohol-seeking behavior is associated with changes in the activation state (e.g., phosphorylation) of CaMKII-T286. Male C57BL/6J mice (n=14) were trained to lever press on a fixed-ratio-4 schedule of sweetened alcohol (2% sucrose+9% EtOH) reinforcement. After 14-d of extinction (no cues or reinforcers), mice underwent a response-contingent reinstatement (n=7) vs. an additional day of extinction (n=7). Brains were removed immediately after the test and processed for evaluation of pCaMKII-T286 immunoreactivity (IR). Number of pCaMKII-T286 positive cells/mm

Indexed as

CuesRewardAnimalsBehavior, AnimalBrainCalcium-Calmodulin-Dependent Protein Kinase Type 2EthanolMaleMiceMice, Inbred C57BLPhosphorylationCalcium-Calmodulin-Dependent Protein Kinase Type 2EthanolAddictionAlcoholAmygdalaCaMKIICaMKII-T286Cue-inducedEthanol olfactoryHabenulaHypothalamusNucleus accumbensPiriform cortexReinstatementRelapseStriatumThalamus

Identifiers

PMID29100991
PMCPMC5779622

What OpenQuestion holds

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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.