Evidence map›Paper›PMID 21734280›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Glial cell line-derived neurotrophic factor reverses alcohol-induced allostasis of the mesolimbic dopaminergic system: implications for alcohol reward and seeking.

Segev Barak, Sebastien Carnicella, Quinn V Yowell, Dorit Ron

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Development of the Neuroimmune Modulator Ibudilast for the Treatment of Alcoholism: A Randomized, Placebo-Controlled, Human Laboratory Trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Trial
  3. The influence of drug class on reward in substance use disorders.Pharmacology, biochemistry, and behavior · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Growth Factors and Alcohol Use Disorder.Cold Spring Harbor perspectives in medicine · 2020
    Review
  9. Review
  10. Review
  11. Receptor Tyrosine Kinases as Therapeutic Targets for Alcohol Use Disorder.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2020
    Review
  12. Inhibition of FGF Receptor-1 Suppresses Alcohol Consumption: Role of PI3 Kinase Signaling in Dorsomedial Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  13. Association of GDNF and CNTNAP2 gene variants with gambling.Journal of behavioral addictions · 2019
    Article
  14. Article
  15. Article
  16. Human Endogenous Retrovirus-K HML-2 integration withinProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  17. Review
  18. Article
  19. Article
  20. Fibroblast Growth Factor 2 in the Dorsomedial Striatum Is a Novel Positive Regulator of Alcohol Consumption.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Segev BarakThe Ernest Gallo Research Center, Department of Neurology, University of California, San Francisco, Emeryville, California 94608, USA.
Sebastien Carnicella
Quinn V Yowell
Dorit Ron
University of California, San Francisco · USErnest Gallo Clinic and Research Center · US

Funding

The Neurotrophic Factor GDNF and Alcohol AddictionR01AA014366 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2004 to 2013
$3.3M
NIAAA NIH HHS R01 AA014366
6 · The paper itself

Abstract

We previously showed that infusion of glial cell line-derived neurotrophic factor (GDNF) into the ventral tegmental area (VTA) rapidly reduces alcohol intake and relapse (Carnicella et al., 2008, 2009a), and increases dopamine (DA) levels in the nucleus accumbens (NAc) of alcohol-naive rats (Wang et al., 2010). Withdrawal from excessive alcohol intake is associated with a reduction in NAc DA levels, whereas drug-induced increases in NAc DA levels are associated with reward. We therefore tested whether GDNF in the VTA reverses alcohol withdrawal-associated DA deficiency and/or possesses rewarding properties. Rats were trained for 7 weeks to consume high levels of alcohol (5.47 ± 0.37 g/kg/24 h) in intermittent access to 20% alcohol in a two-bottle choice procedure. Using in vivo microdialysis, we show that 24 h withdrawal from alcohol causes a substantial reduction in NAc DA overflow, which was reversed by intra-VTA GDNF infusion. Using conditioned place preference (CPP) paradigm, we observed that GDNF on its own does not induce CPP, suggesting that the growth factor is not rewarding. However, GDNF blocked acquisition and expression of alcohol-CPP. In addition, GDNF induced a downward shift in the dose-response curve for operant self-administration of alcohol, further suggesting that GDNF suppresses, rather than substitutes for, the reinforcing effects of alcohol. Our findings suggest that GDNF reduces alcohol-drinking behaviors by reversing an alcohol-induced allostatic DA deficiency in the mesolimbic system. In addition, as it lacks abuse liability, the study further highlights GDNF as a promising target for treatment of alcohol use/abuse disorders.

Indexed as

RewardAlcohol DrinkingAlcoholsAllostasisAnimalsChoice BehaviorConditioning, OperantDopamineDose-Response Relationship, DrugGlial Cell Line-Derived Neurotrophic FactorLimbic SystemMaleMicrodialysisModels, BiologicalMotor ActivityRatsAlcoholsDopamineGlial Cell Line-Derived Neurotrophic Factor

Identifiers

PMID21734280
PMCPMC3144766
OpenAlexW2055390989

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.