Evidence map›Paper›PMID 24005290›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Protein tyrosine phosphatase α in the dorsomedial striatum promotes excessive ethanol-drinking behaviors.

Sami Ben Hamida, Emmanuel Darcq, Jun Wang, Su Wu, Khanhky Phamluong, Viktor Kharazia, Dorit Ron

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Neuregulin 3 Signaling Mediates Nicotine-Dependent Synaptic Plasticity in the Orbitofrontal Cortex and Cognition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Alcohol dependence: molecular and behavioral evidence.Trends in pharmacological sciences · 2014
    Review
  19. Article
  20. Neurochemical mechanisms of alcohol withdrawal.Handbook of clinical neurology · 2014
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Sami Ben HamidaGallo Center at the Department of Neurology, University of California, San Francisco, San Francisco, California 94143, USA.
Emmanuel Darcq
Jun Wang
Su Wu
Khanhky Phamluong
Viktor Kharazia
Dorit Ron
Ernest Gallo Clinic and Research Center · USUniversity of California, San Francisco · US

Funding

Vector, Transgenic, and Imaging CoreP50AA017072 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2008 to 2017
$13.9M
Phosphorylation and the CNS Actions of EthanolR01AA013438 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2002 to 2012
$3.7M
NIAAA NIH HHS P50 AA017072NIAAA NIH HHS R01 AA013438NIAAA NIH HHS R01AA 013438
6 · The paper itself

Abstract

We previously found that excessive ethanol drinking activates Fyn in the dorsomedial striatum (DMS) (Wang et al., 2010; Gibb et al., 2011). Ethanol-mediated Fyn activation in the DMS leads to the phosphorylation of the GluN2B subunit of the NMDA receptor, to the enhancement of the channel's activity, and to the development and/or maintenance of ethanol drinking behaviors (Wang et al., 2007, 2010). Protein tyrosine phosphatase α (PTPα) is essential for Fyn kinase activation (Bhandari et al., 1998), and we showed that ethanol-mediated Fyn activation is facilitated by the recruitment of PTPα to synaptic membranes, the compartment where Fyn resides (Gibb et al., 2011). Here we tested the hypothesis that PTPα in the DMS is part of the Fyn/GluN2B pathway and is thus a major contributor to the neuroadaptations underlying excessive ethanol intake behaviors. We found that RNA interference (RNAi)-mediated PTPα knockdown in the DMS reduces excessive ethanol intake and preference in rodents. Importantly, no alterations in water, saccharine/sucrose, or quinine intake were observed. Furthermore, downregulation of PTPα in the DMS of mice significantly reduces ethanol-mediated Fyn activation, GluN2B phosphorylation, and ethanol withdrawal-induced long-term facilitation of NMDAR activity without altering the intrinsic features of DMS neurons. Together, these results position PTPα upstream of Fyn within the DMS and demonstrate the important contribution of the phosphatase to the maladaptive synaptic changes that lead to excessive ethanol intake.

Indexed as

Adaptation, PhysiologicalAlcohol DrinkingAnimalsCorpus StriatumDown-RegulationMaleMiceMice, Inbred C57BLNeuronsPhosphorylationProto-Oncogene Proteins c-fynRatsRats, Long-EvansReceptor-Like Protein Tyrosine Phosphatases, Class 4Receptors, N-Methyl-D-AspartateTranscription, GeneticNR2B NMDA receptorProto-Oncogene Proteins c-fynReceptor-Like Protein Tyrosine Phosphatases, Class 4Receptors, N-Methyl-D-Aspartate

Identifiers

PMID24005290
PMCPMC3761047
OpenAlexW1994669704

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.