Evidence map›Paper›PMID 26247621›Full record

ArticleAlcoholism, clinical and experimental research2015

CaMKIIα-GluA1 Activity Underlies Vulnerability to Adolescent Binge Alcohol Drinking.

Abigail E Agoglia, Sarah E Holstein, Grant Reid, Clyde W Hodge

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 27% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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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

4 authors at 1 institution in 1 country.

Abigail E AgogliaBowles Center for Alcohol Studies, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina.
Sarah E HolsteinBowles Center for Alcohol Studies, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina.
Grant ReidBowles Center for Alcohol Studies, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina.
Clyde W HodgeBowles Center for Alcohol Studies, University of North Carolina, Chapel Hill, Chapel Hill, North Carolina.
University of North Carolina at Chapel Hill · US

Funding

UNC ARC Information/Dissemination CoreP60AA011605 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Melissa A Herman · 2003 to 2026
$46.3M
Molecular Mechanisms of Ethanol Reinforcement R37AA014983 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HODGE, CLYDE W · 2013 to 2020
$2.7M
Molecular Mechanisms of Ethanol ReinforcementR01AA014983 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI HODGE, CLYDE W · 2005 to 2012
$2.0M
Assessing the adolescent PFC proteome for mechanisms of escalated alcohol self-administration in adulthoodF31AA024375 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI AGOGLIA, ABIGAIL ELIZABETH · 2015 to 2016
$63k
NIAAA NIH HHS F31 AA024375NIAAA NIH HHS P60 AA011605NIAAA NIH HHS P60AA11605NIAAA NIH HHS R01 AA014983NIAAA NIH HHS R37 AA014983NIAAA NIH HHS R37AA014983
6 · The paper itself

Abstract

backgroundBinge drinking during adolescence is associated with increased risk for developing alcohol use disorders; however, the neural mechanisms underlying this liability are unclear. In this study, we sought to determine whether binge drinking alters expression or phosphorylation of 2 molecular mechanisms of neuroplasticity, calcium/calmodulin-dependent kinase II alpha (CaMKIIα) and the GluA1 subunit of AMPA receptors (AMPARs) in addiction-associated brain regions. We also asked whether activation of CaMKIIα-dependent AMPAR activity escalates binge-like drinking.

methodsTo address these questions, CaMKIIαT286 and GluA1S831 protein phosphorylation and expression were assessed in the amygdala and striatum of adolescent and adult male C57BL/6J mice immediately after voluntary binge-like alcohol drinking (blood alcohol >80 mg/dl). In separate mice, effects of the CaMKIIα-dependent GluA1S831 phosphorylation (pGluA1S831 )-enhancing drug tianeptine were tested on binge-like alcohol consumption in both age groups.

resultsBinge-like drinking decreased CaMKIIαT286 phosphorylation (pCaMKIIαT286 ) selectively in adolescent amygdala with no effect in adults. Alcohol also produced a trend for reduced pGluA1S831 expression in adolescent amygdala but differentially increased pGluA1S831 in adult amygdala. No effects were observed in the nucleus accumbens or dorsal striatum. Tianeptine increased binge-like alcohol consumption in adolescents but decreased alcohol consumption in adults. Sucrose consumption was similarly decreased by tianeptine pretreatment in both ages.

conclusionsThese data show that the adolescent and adult amygdalae are differentially sensitive to effects of binge-like alcohol drinking on plasticity-linked glutamate signaling molecules. Tianeptine-induced increases in binge-like drinking only in adolescents suggest that differential CaMKIIα-dependent AMPAR activation may underlie age-related escalation of binge drinking.

Indexed as

Age FactorsAmygdalaAnimalsBinge DrinkingCalcium-Calmodulin-Dependent Protein Kinase Type 2EthanolMaleMiceMice, Inbred C57BLReceptors, AMPAThiazepinesCalcium-Calmodulin-Dependent Protein Kinase Type 2EthanolReceptors, AMPAThiazepinestianeptineAdolescenceAlcoholBingeCaMKIIGluA1

Identifiers

PMID26247621
PMCPMC4558330
OpenAlexW1897099154

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.