Evidence map›Paper›PMID 26202104›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016

Neuroimmune Regulation of GABAergic Neurons Within the Ventral Tegmental Area During Withdrawal from Chronic Morphine.

Anna M W Taylor, Annie Castonguay, Atefeh Ghogha, Pia Vayssiere, Amynah A A Pradhan, Lihua Xue, Sadaf Mehrabani, Juli Wu, Pat Levitt, Mary C Olmstead and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 109 citations in OpenAlex.

  1. Article
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  11. Article
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  13. Article
  14. Substance Use and Addiction.Advances in neurobiology · 2024
    Review
  15. Article
  16. Ventral tegmental area glutamate neurons establish a mu-opioid receptor gated circuit to mesolimbic dopamine neurons and regulate opioid-seeking behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
  17. Article
  18. Review
  19. Effects of GABAResearch in pharmaceutical sciences · 2023
    Article
  20. Role of Microglia in Psychostimulant Addiction.Current neuropharmacology · 2023
    Review

10 more citing papers are in PubMed but not listed here.

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

13 authors at 5 institutions in 2 countries.

Anna M W TaylorDepartment of Anesthesiology and Perioperative Care, University of California, Irvine, CA, USA.
Annie CastonguayInstitut Universitaire en Santé Mentale de Québec, Québec, QC, Canada.
Atefeh GhoghaHatos Center for Neuropharmacology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Pia VayssiereHatos Center for Neuropharmacology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Amynah A A PradhanHatos Center for Neuropharmacology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Lihua XueDepartment of Biomedical and Molecular Sciences, Queen's University, Kingston, ON, Canada.
Sadaf MehrabaniHatos Center for Neuropharmacology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Juli WuChildren's Hospital Los Angeles and the Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.
Pat LevittChildren's Hospital Los Angeles and the Keck School of Medicine of the University of Southern California, Los Angeles, CA, USA.
Mary C OlmsteadDepartment of Psychology, Queen's University, Kingston, ON, Canada.
Yves De KoninckInstitut Universitaire en Santé Mentale de Québec, Québec, QC, Canada.ORCID http://orcid.org/0000-0002-5779-9330
Christopher J EvansHatos Center for Neuropharmacology, Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, CA, USA.
Catherine M CahillDepartment of Anesthesiology and Perioperative Care, University of California, Irvine, CA, USA.
University of California, Los Angeles · USInstitut Universitaire en Santé Mentale de Québec · CAQueen's University · CAUniversity of Southern California · USUniversity of California, Irvine · US

Funding

The Role of Striosome Neurons in Mediating Opiod RewardP50DA005010 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FANSELOW, MICHAEL S · 1987 to 2021
$30.7M
In Vivo Implications of Agonist Selective Activation of Delta Opioid ReceptorR00DA031243 · NIDA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PRADHAN, AMYNAH AMIR ALI · 2013 to 2015
$743k
In Vivo Implications of Agonist Selective Activation of Delta Opioid ReceptorK99DA031243 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI PRADHAN, AMYNAH AMIR ALI · 2011 to 2012
$317k
Canadian Institutes of Health Research MOP 123298Canadian Institutes of Health Research MOP 12942NIDA NIH HHS K99 DA031243NIDA NIH HHS P50 DA005010NIDA NIH HHS R00 DA031243
6 · The paper itself

Abstract

Opioid dependence is accompanied by neuroplastic changes in reward circuitry leading to a negative affective state contributing to addictive behaviors and risk of relapse. The current study presents a neuroimmune mechanism through which chronic opioids disrupt the ventral tegmental area (VTA) dopaminergic circuitry that contributes to impaired reward behavior. Opioid dependence was induced in rodents by treatment with escalating doses of morphine. Microglial activation was observed in the VTA following spontaneous withdrawal from chronic morphine treatment. Opioid-induced microglial activation resulted in an increase in brain-derived neurotrophic factor (BDNF) expression and a reduction in the expression and function of the K(+)Cl(-) co-transporter KCC2 within VTA GABAergic neurons. Inhibition of microglial activation or interfering with BDNF signaling prevented the loss of Cl(-) extrusion capacity and restored the rewarding effects of cocaine in opioid-dependent animals. Consistent with a microglial-derived BDNF-induced disruption of reward, intra-VTA injection of BDNF or a KCC2 inhibitor resulted in a loss of cocaine-induced place preference in opioid-naïve animals. The loss of the extracellular Cl(-) gradient undermines GABAA-mediated inhibition, and represents a mechanism by which chronic opioid treatments can result in blunted reward circuitry. This study directly implicates microglial-derived BDNF as a negative regulator of reward in opioid-dependent states, identifying new therapeutic targets for opiate addictive behaviors.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCocaineGABAergic NeuronsK Cl- CotransportersMaleMiceMice, Inbred C57BLMicrogliaModels, NeurologicalMorphineNeuroimmunomodulationRewardSubstance Withdrawal SyndromeSymportersVentral Thalamic NucleiBrain-Derived Neurotrophic FactorCocaineK Cl- CotransportersMorphineSymporters

Identifiers

PMID26202104
PMCPMC4748420
OpenAlexW962591458

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.