Evidence map›Paper›PMID 18412612›Full record

ArticleThe European journal of neuroscience2008

Neuroplasticity in brain reward circuitry following a history of ethanol dependence.

Anita C Hansson, Roberto Rimondini, Olga Neznanova, Wolfgang H Sommer, Markus Heilig

Open access · greenAbstract read
In one paragraph

Article in The European journal of neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Identifying neurobiological phenotypes associated with alcohol use disorder severity.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    Trial
  4. Review
  5. Neural Circuitries and Alcohol Use Disorder: Cutting Corners in the Cycle.Current topics in behavioral neurosciences · 2025
    Review
  6. Molecular mechanisms of alcohol's effects on the human body: A review and update.Journal of biochemical and molecular toxicology · 2023
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. The role of the orbitofrontal cortex in alcohol use, abuse, and dependence.Progress in neuro-psychopharmacology & biological psychiatry · 2018
    Review
  19. Article
  20. 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 2 institutions in 2 countries.

Anita C HanssonLaboratory of Clinical and Translational Studies, NIAAA/NIH, Bethesda, MD 20892-1108, USA. anita.hansson@mail.nih.gov
Roberto Rimondini
Olga Neznanova
Wolfgang H Sommer
Markus Heilig
National Institutes of Health · USUniversity of Bologna · IT

Funding

Intramural NIH HHS NIH0012006624
6 · The paper itself

Abstract

Mitogen-activated and extracellular regulated kinase (MEK) and extracellular signal-regulated protein kinase (ERK) pathways may underlie ethanol-induced neuroplasticity. Here, we used the MEK inhibitor 1,4-diamino-2,3-dicyano-1,4-bis(2-aminophenylthio)butadiene (UO126) to probe the role of MEK/ERK signaling for the cellular response to an acute ethanol challenge in rats with or without a history of ethanol dependence. Ethanol (1.5 g/kg, i.p.) induced expression of the marker genes c-fos and egr-1 in brain regions associated with both rewarding and stressful ethanol actions. Under non-dependent conditions, ethanol-induced c-fos expression was generally not affected by MEK inhibition, with the exception of the medial amygdala (MeA). In contrast, following a history of dependence, a markedly suppressed c-fos response to acute ethanol was found in the medial pre-frontal/orbitofrontal cortex (OFC), nucleus accumbens shell (AcbSh) and paraventricular nucleus (PVN). The suppressed ethanol response in the OFC and AcbSh, key regions involved in ethanol preference and seeking, was restored by pre-treatment with UO126, demonstrating a recruitment of an ERK/MEK-mediated inhibitory regulation in the post-dependent state. Conversely, in brain areas involved in stress responses (MeA and PVN), an MEK/ERK-mediated cellular activation by acute ethanol was lost following a history of dependence. These data reveal region-specific neuroadaptations encompassing the MEK/ERK pathway in ethanol dependence. Recruitment of MEK/ERK-mediated suppression of the ethanol response in the OFC and AcbSh may reflect devaluation of ethanol as a reinforcer, whereas loss of an MEK/ERK-mediated response in the MeA and PVN may reflect tolerance to its aversive actions. These two neuroadaptations could act in concert to facilitate progression into ethanol dependence.

Indexed as

RewardAlcoholismAnimalsBrainButadienesCentral Nervous System DepressantsEarly Growth Response Protein 1Enzyme InhibitorsEthanolGene ExpressionGenes, fosImmunohistochemistryIn Situ HybridizationMaleMAP Kinase Kinase KinasesNeuronal PlasticityButadienesCentral Nervous System DepressantsEarly Growth Response Protein 1Egr1 protein, ratEnzyme InhibitorsEthanolMAP Kinase Kinase KinasesNitrilesU 0126

Identifiers

PMID18412612
PMCPMC2486413
OpenAlexW1982871940

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.