Evidence map›Paper›PMID 19258026›Full record

ArticleNeuroscience2009

Ethanol-induced delta-opioid receptor modulation of glutamate synaptic transmission and conditioned place preference in central amygdala.

B Bie, W Zhu, Z Z Pan

Abstract read
In one paragraph

Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

27 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Tryptophan Substitution in CJ-15,208 (Pharmaceuticals (Basel, Switzerland) · 2023
    Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. The amygdalar opioid system.Handbook of behavioral neuroscience · 2020
    Article
  9. Review
  10. Article
  11. Article
  12. Delta Opioid Pharmacology in Relation to Alcohol Behaviors.Handbook of experimental pharmacology · 2018
    Review
  13. Review
  14. Article
  15. Molecular Pharmacology of δ-Opioid Receptors.Pharmacological reviews · 2016
    Review
  16. Review
  17. MeCP2 repression of G9a in regulation of pain and morphine reward.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

B BieDepartment of Anesthesiology and Pain Medicine, The University of Texas-MD Anderson Cancer Center, 1515 Holcombe Boulevard, Unit 110, Houston, TX 77030, USA.
W Zhu
Z Z Pan
The University of Texas MD Anderson Cancer Center · US

Funding

Delta-Opioid Receptor Trafficking and Pain InhibitionR01DA023069 · NIDA · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PAN, ZHIZHONG Z. · 2008 to 2012
$1.5M
Opioid Receptors in the Mechanisms of Opioid ToleranceR01DA014524 · NIDA · UNIVERSITY OF TEXAS MD ANDERSON CAN CTR · PI PAN, ZHIZHONG Z · 2001 to 2005
$1.3M
NIDA NIH HHS DA014524NIDA NIH HHS DA023069NIDA NIH HHS R01 DA014524NIDA NIH HHS R01 DA023069
6 · The paper itself

Abstract

Alcoholism involves compulsive behaviors of alcohol drinking, which is thought to be related at least initially to the rewarding effect of alcohol. It has been shown that mu-opioid receptors play an essential role in drug reward and dependence for many drugs of abuse including alcohol, but the function of delta-opioid receptors (DOR) in drug reward remains largely unknown at present. Previous animal studies using systemic approaches with DOR antagonists or DOR knockout animals have yielded inconsistent results, showing a decrease, an increase or no change in alcohol consumption and behaviors of alcohol reward after DOR inhibition or deletion. In the present study, we used ethanol-conditioned rats to investigate adaptive DOR function in neurons of the central nucleus of the amygdala (CeA), a key brain site for alcohol reward and addiction. We found that functional DOR was absent in glutamate synapses of CeA neurons from control rats, but it emerged and inhibited glutamate synaptic currents in CeA neurons from rats displaying ethanol-induced behavior of conditioned place preference (CPP). Analysis of paired-pulse ratios and miniature glutamate synaptic currents revealed that the recruited DOR was present on glutamatergic presynaptic terminals. Similar induction of functional DOR was also found on GABA synapses. Furthermore, microinjection of a DOR antagonist into the CeA reversed ethanol-induced CPP behavior in rats in vivo. These results suggest that repeated alcohol exposure recruits new functional DOR on CeA glutamate and GABA synapses, which may be involved in the expression or maintenance of ethanol-induced CPP behavior.

Indexed as

Adaptation, PhysiologicalAmygdalaAnimalsAssociation LearningCentral Nervous System DepressantsConditioning, ClassicalEthanolgamma-Aminobutyric AcidGlutamic AcidIn Vitro TechniquesMalePatch-Clamp TechniquesRandom AllocationRatsRats, WistarReceptors, Opioid, deltaCentral Nervous System DepressantsEthanolgamma-Aminobutyric AcidGlutamic AcidReceptors, Opioid, delta

Identifiers

PMID19258026
PMCPMC2669697
OpenAlexW1974156675

What OpenQuestion holds

Textmetadata
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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.