Evidence map›Paper›PMID 20393452›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2010

Ethanol blocks long-term potentiation of GABAergic synapses in the ventral tegmental area involving mu-opioid receptors.

Yan-zhong Guan, Jiang-Hong Ye

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
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

39 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  4. Frontiers in psychiatry · 2023
    Review
  5. Article
  6. Article
  7. Article
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  11. Article
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  15. Dopamine and addiction: what have we learned from 40 years of research.Journal of neural transmission (Vienna, Austria : 1996) · 2019
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  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

2 authors at 1 institution in 1 country.

Yan-zhong GuanDepartment of Anesthesiology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark, NJ 07103, USA.
Jiang-Hong Ye
Rutgers New Jersey Medical School

Funding

Alcohol and mesolimbic glutamatergic transmissionsR01AA016964 · NIAAA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI YE, JIANG-HONG · 2008 to 2011
$1.4M
Glycine regulates ethanol intakeR21AA016618 · NIAAA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI YE, JIANG-HONG · 2010 to 2011
$431k
Ethanol and mesolimbic GABAergic neuronsR21AA015925 · NIAAA · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI YE, JIANG-HONG · 2006 to 2007
$403k
NIAAA NIH HHS R01 AA016964NIAAA NIH HHS R01AA016964NIAAA NIH HHS R21 AA015925NIAAA NIH HHS R21AA015925NIAAA NIH HHS R21 AA016618NIAAA NIH HHS R21AA016618
6 · The paper itself

Abstract

It is well documented that ethanol exposure alters GABA (gamma-aminobutyric acid)-releasing synapses, and ethanol addiction is associated with endogenous opioid system. Emerging evidence indicates that opioids block long-term potentiation in the fast inhibitory GABA(A) receptor synapses (LTP(GABA)) onto dopamine-containing neurons in the ventral tegmental area (VTA), a brain region essential for reward-seeking behavior. However, how ethanol affects LTP(GABA) is not known. We report here that in acute midbrain slices from rats, clinically relevant concentrations of ethanol applied both in vitro and in vivo prevents LTP(GABA), which is reversed, respectively, by in vitro and in vivo administration of naloxone, a mu-opioid receptor (MOR) antagonist. Furthermore, the blockade of LTP(GABA) induced by a brief in vitro ethanol treatment is mimicked by DAMGO ([D-Ala(2), N-MePhe(4), Gly-ol]-enkephalin), a MOR agonist. Paired-pulse ratios are similar in slices, 24 h after in vivo injection with either saline or ethanol. Sp-cAMPS, a stable cAMP analog, and pCPT-cGMP, a cGMP analog, potentiates GABA(A)-mediated inhibitory postsynaptic currents in slices from ethanol-treated rats, indicating that a single in vivo ethanol exposure does not maximally increase GABA release, instead, ethanol produces a long-lasting inability to generate LTP(GABA). These neuroadaptations to ethanol might contribute to early stage of addiction.

Indexed as

Analgesics, OpioidAnimalsAnimals, NewbornCentral Nervous System DepressantsCyclic AMPCyclic GMPDopamineElectric StimulationEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Enzyme InhibitorsEthanolgamma-Aminobutyric AcidInhibitory Postsynaptic PotentialsIn Vitro TechniquesLong-Term PotentiationNeuronsadenosine-3',5'-cyclic phosphorothioateAnalgesics, OpioidCentral Nervous System DepressantsCPT-cGMPCyclic AMPCyclic GMPDopamineEnkephalin, Ala(2)-MePhe(4)-Gly(5)-Enzyme InhibitorsEthanolgamma-Aminobutyric AcidReceptors, Opioid, muThionucleotides

Identifiers

PMID20393452
PMCPMC2904870
OpenAlexW2014410471

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.