Evidence map›Paper›PMID 25278838›Full record

ArticleFrontiers in cellular neuroscience2014

Expression of specific ionotropic glutamate and GABA-A receptor subunits is decreased in central amygdala of alcoholics.

Zhe Jin, Amol K Bhandage, Igor Bazov, Olga Kononenko, Georgy Bakalkin, Esa R Korpi, Bryndis Birnir

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Regulation of GABAInternational journal of molecular sciences · 2020
    Review
  11. Review
  12. Review
  13. Article
  14. GABAPsychopharmacology · 2018
    Review
  15. Examining the effects of alcohol on GABAAlcohol (Fayetteville, N.Y.) · 2018
    Article
  16. Article
  17. Article
  18. Article
  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

7 authors at 2 institutions in 2 countries.

Zhe JinMolecular Physiology and Neuroscience Unit, Neuroscience, Biomedical Center, Uppsala University Uppsala, Sweden.
Amol K BhandageMolecular Physiology and Neuroscience Unit, Neuroscience, Biomedical Center, Uppsala University Uppsala, Sweden.
Igor BazovDivision of Biological Research on Drug Dependence, Department of Pharmaceutical Biosciences, Uppsala University Uppsala, Sweden.
Olga KononenkoDivision of Biological Research on Drug Dependence, Department of Pharmaceutical Biosciences, Uppsala University Uppsala, Sweden.
Georgy BakalkinDivision of Biological Research on Drug Dependence, Department of Pharmaceutical Biosciences, Uppsala University Uppsala, Sweden.
Esa R KorpiPharmacology, Institute of Biomedicine, University of Helsinki Helsinki, Finland.
Bryndis BirnirMolecular Physiology and Neuroscience Unit, Neuroscience, Biomedical Center, Uppsala University Uppsala, Sweden.
Uppsala University · SEUniversity of Helsinki · FI

Funding

Brain Tissue Resource Centre for Alcohol ResearchR28AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI Greg Trevor Sutherland · 2012 to 2026
$7.0M
BRAIN TISSUE RESOURCE CENTER FOR ALCOHOL RESEARCHR24AA012725 · NIAAA · UNIVERSITY OF SYDNEY · PI KRIL, JILLIAN JUNE · 2000 to 2011
$2.2M
NIAAA NIH HHS R24 AA012725NIAAA NIH HHS R28 AA012725
6 · The paper itself

Abstract

The central amygdala (CeA) has a role for mediating fear and anxiety responses. It is also involved in emotional imbalance caused by alcohol abuse and dependence and in regulating relapse to alcohol abuse. Growing evidences suggest that excitatory glutamatergic and inhibitory γ-aminobutyric acid-ergic (GABAergic) transmissions in the CeA are affected by chronic alcohol exposure. Human post-mortem CeA samples from male alcoholics (n = 9) and matched controls (n = 9) were assayed for the expression level of ionotropic glutamate and GABA-A receptors subunit mRNAs using quantitative real-time reverse transcription-PCR (RT-qPCR). Our data revealed that out of the 16 ionotropic glutamate receptor subunits, mRNAs encoding two AMPA [2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl)propanoic acid] receptor subunits GluA1 and GluA4; one kainate receptor subunit GluK2; one NMDA (N-methyl-D-aspartate) receptor subunit GluN2D and one delta receptor subunit GluD2 were significantly decreased in the CeA of alcoholics. In contrast, of the 19 GABA-A receptor subunits, only the mRNA encoding the α2 subunit was significantly down-regulated in the CeA of the alcoholics as compared with control subjects. Our findings imply that the down-regulation of specific ionotropic glutamate and GABA-A receptor subunits in the CeA of alcoholics may represent one of the molecular substrates underlying the new balance between excitatory and inhibitory neurotransmission in alcohol dependence.

Indexed as

alcohol dependenceamygdalabrainGABAA receptorionotropic glutamate receptorspost-mortem

Identifiers

PMID25278838
PMCPMC4165314
OpenAlexW2148261020

What OpenQuestion holds

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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.