Evidence map›Paper›PMID 24710789›Full record

ArticleNeurochemical research2014

Ethanol-induced plasticity of GABAA receptors in the basolateral amygdala.

A Kerstin Lindemeyer, Jing Liang, Vincent N Marty, Edward M Meyer, Asha Suryanarayanan, Richard W Olsen, Igor Spigelman

Open access · greenAbstract read
In one paragraph

Article in Neurochemical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Intoxicating effects of alcohol depend on acid-sensing ion channels.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Role of Hippocampal Neurogenesis in Alcohol Withdrawal Seizures.Brain plasticity (Amsterdam, Netherlands) · 2020
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Role of GABAMolecular brain · 2017
    Review
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 1 institution in 1 country.

A Kerstin LindemeyerDepartment of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, Los Angeles, CA, USA.
Jing Liang
Vincent N Marty
Edward M Meyer
Asha Suryanarayanan
Richard W Olsen
Igor Spigelman
University of California, Los Angeles · US

Funding

Mechanisms of GABAA Receptor Plasticity in AlcoholismR01AA016100 · NIAAA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SPIGELMAN, IGOR · 2007 to 2011
$1.7M
NIAAA NIH HHS R01 AA016100
6 · The paper itself

Abstract

Acute and chronic ethanol (EtOH) administration is known to affect function, surface expression, and subunit composition of γ-aminobutyric acid (A) receptors (GABAARs) in different parts of the brain, which is believed to play a major role in alcohol dependence and withdrawal symptoms. The basolateral amygdala (BLA) participates in anxiety-like behaviors including those induced by alcohol withdrawal. In the present study we assessed the changes in cell surface levels of select GABAAR subunits in the BLA of a rat model of alcohol dependence induced by chronic intermittent EtOH (CIE) treatment and long-term (>40 days) withdrawal and investigated the time-course of such changes after a single dose of EtOH (5 g/kg, gavage). We found an early decrease in surface expression of α4 and δ subunits at 1 h following single dose EtOH treatment. At 48 h post-EtOH and after CIE treatment there was an increase in α4 and γ2, while α1, α2, and δ surface expression were decreased. To relate functional changes in GABAARs to changes in their subunit composition we analyzed miniature inhibitory postsynaptic currents (mIPSCs) and the picrotoxin-sensitive tonic current (Itonic) 48 h after EtOH intoxication. The Itonic magnitude and most of the mIPSC kinetic parameters (except faster mIPSC decay) were unchanged at 48 h post-EtOH. At the same time, Itonic potentiation by acute EtOH was greatly reduced, whereas mIPSCs became significantly more sensitive to potentiation by acute EtOH. These results suggest that EtOH intoxication-induced GABAAR plasticity in the BLA might contribute to the diminished sedative/hypnotic and maintained anxiolytic effectiveness of EtOH.

Indexed as

AnimalsBasolateral Nuclear ComplexEthanolMaleNeuronal PlasticityRatsRats, Sprague-DawleyReceptors, GABA-AEthanolReceptors, GABA-A

Identifiers

PMID24710789
PMCPMC4121120
OpenAlexW2064794291

What OpenQuestion holds

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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.