Evidence map›Paper›PMID 23459588›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013

αCaMKII autophosphorylation controls the establishment of alcohol drinking behavior.

Alanna C Easton, Walter Lucchesi, Anbarasu Lourdusamy, Bernd Lenz, Jalal Solati, Yulia Golub, Piotr Lewczuk, Cathy Fernandes, Sylvane Desrivieres, Ralph R Dawirs and 30 more

Erratum issuedOpen 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. An erratum has been issued. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  8. Ras GEF Mouse Models for the Analysis of Ras Biology and Signaling.Methods in molecular biology (Clifton, N.J.) · 2021
    Article
  9. Effects of nicotine on DARPP-32 and CaMKII signaling relevant to addiction.Advances in pharmacology (San Diego, Calif.) · 2021
    Review
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

40 authors at 8 institutions in 3 countries.

Alanna C EastonMRC Social, Genetic and Developmental Psychiatry Research Centre, Institute of Psychiatry, King's College London, London, UK.
Walter Lucchesi
Anbarasu Lourdusamy
Bernd Lenz
Jalal Solati
Yulia Golub
Piotr Lewczuk
Cathy Fernandes
Sylvane Desrivieres
Ralph R Dawirs
Gunther H Moll
Johannes Kornhuber
Josef Frank
Per Hoffmann
Michael Soyka
Falk Kiefer
GESGA Consortium
Gunter Schumann
K Peter Giese
Christian P Müller
Jens Treutlein
Sven Cichon
Monika Ridinger
Peter Mattheisen
Stefan Herms
Norbert Wodarz
Peter Zill
Wolfgang Maier
Rainald Mössner
Wolfgang Gaebel
Norbert Dahmen
Norbert Scherbaum
Christine Schmäl
Michael Steffens
Susanne Lucae
Marcus Ising
Bertram Müller-Myhsok
Markus M Nöthen
Karl Mann
Marcella Rietschel
King's College London · GBFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversitätsklinikum Erlangen · DEHeidelberg University · DEIslamic Azad University, Karaj · IRLudwig-Maximilians-Universität München · DEUniversity Hospital Heidelberg · DEUniversity of Bonn · DE

Funding

Medical Research Council G0800393Medical Research Council G0901858
6 · The paper itself

Abstract

The α-Ca(2+)/calmodulin-dependent protein kinase II (αCaMKII) is a crucial enzyme controlling plasticity in the brain. The autophosphorylation of αCaMKII works as a 'molecular memory' for a transient calcium activation, thereby accelerating learning. We investigated the role of αCaMKII autophosphorylation in the establishment of alcohol drinking as an addiction-related behavior in mice. We found that alcohol drinking was initially diminished in αCaMKII autophosphorylation-deficient αCaMKII(T286A) mice, but could be established at wild-type level after repeated withdrawals. The locomotor activating effects of a low-dose alcohol (2 g/kg) were absent in αCaMKII(T286A) mice, whereas the sedating effects of high-dose (3.5 g/kg) were preserved after acute and subchronic administration. The in vivo microdialysis revealed that αCaMKII(T286A) mice showed no dopamine (DA) response in the nucleus accumbens to acute or subchronic alcohol administration, but enhanced serotonin (5-HT) responses in the prefrontal cortex. The attenuated DA response in αCaMKII(T286A) mice was in line with altered c-Fos activation in the ventral tegmental area after acute and subchronic alcohol administration. In order to compare findings in mice with the human condition, we tested 23 single-nucleotide polymorphisms (SNPs) in the CAMK2A gene for their association with alcohol dependence in a population of 1333 male patients with severe alcohol dependence and 939 controls. We found seven significant associations between CAMK2A SNPs and alcohol dependence, one of which in an autophosphorylation-related area of the gene. Together, our data suggest αCaMKII autophosphorylation as a facilitating mechanism in the establishment of alcohol drinking behavior with changing the DA-5-HT balance as a putative mechanism.

Indexed as

Alcohol DrinkingAlcoholismAnimalsBehavior, AddictiveCalcium-Calmodulin-Dependent Protein Kinase Type 2Case-Control StudiesDopamineDose-Response Relationship, DrugEthanolFemaleGenetic Predisposition to DiseaseHumansHypnotics and SedativesMaleMiceMotor ActivityCalcium-Calmodulin-Dependent Protein Kinase Type 2CAMK2A protein, humanCamk2a protein, mouseDopamineEthanolHypnotics and SedativesSerotonin

Identifiers

PMID23459588
PMCPMC3717547
OpenAlexW2052925957

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.