Evidence map›Paper›PMID 18551281›Full record

ArticlePsychopharmacology2008

Role of accumbens BDNF and TrkB in cocaine-induced psychomotor sensitization, conditioned-place preference, and reinstatement in rats.

Amine Bahi, Frederic Boyer, Vijay Chandrasekar, Jean-Luc Dreyer

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

69 citing papers in PubMed, 130 citations in OpenAlex.

  1. Article
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  7. Epigenetic Effects of Addictive Drugs in the Nucleus Accumbens.Frontiers in molecular neuroscience · 2022
    Review
  8. Article
  9. Article
  10. Review
  11. Article
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  14. Review
  15. BDNF-TrkB controls cocaine-induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  16. Reward Circuitry in Addiction.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

  • Erratum issued
    Chandrasekar, Vijay [added]
5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Amine BahiDepartment of Psychiatry, Yale University School of Medicine, 301 Cedar Street, New Haven, CT 06508, USA.
Frederic Boyer
Vijay Chandrasekar
Jean-Luc Dreyer
University of Fribourg · CHYale University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBrain-derived neurotrophic factor (BDNF) is involved in the survival and function of midbrain DA neurons. BDNF action is mediated by the TrkB receptor-tyrosine kinase, and both BDNF and TrkB transcripts are widely expressed in the rat mesolimbic pathway, including the nucleus accumbens (NAc) and the ventral tegmentum area (VTA).

objectiveBDNF was previously shown to be involved in cocaine reward and relapse, as assessed in rat models. The goal of this study is to explore the role of BDNF and TrkB in the rat nucleus accumbens (NAc) in cocaine-induced psychomotor sensitization and in conditioned-place preference acquisition, expression, and reinstatement. MATERIALS AND

methodsIn vivo genetic manipulations of BDNF and TrkB were performed using a lentiviral gene delivery approach to over-express these genes in the NAc and siRNA-based technology to locally knockdown gene expression. Behavioral experiments consisted of locomotor activity monitoring or cocaine-induced conditioned-place preference (CPP).

resultsBDNF and/or its receptor TrkB in the NAc enhance drug-induced locomotor activity and induce sensitization in rats. Furthermore, LV-BDNF- and LV-TrkB-treated rats display enhanced cocaine-induced CPP, delayed CPP-extinction upon repeated measurements, and increased CPP reinstatement. In contrast, expression of TrkT1 (truncated form of TrkB, acting as a dominant negative) inhibits these behavioral changes. This inhibition is also observed when rats are fed doxycycline (to block lentivirus-mediated gene expression) or when injected with siRNAs-expressing lentiviruses against TrkB. In addition, we investigate the establishment, maintenance, extinction, and reinstatement of cocaine-induced CPP. We show that BDNF and TrkB-induced CPP takes place during the learning period (conditioning), whereas extinction leads to the loss of CPP. Extinction is delayed when rats are injected LV-BDNF or LV-TrkB, and in turn, priming injections of 2 mg/kg of cocaine reinstates it.

conclusionsThese results demonstrate the crucial function of BDNF-through its receptor TrkB-in the enhancement of locomotor activity, sensitization, conditioned-place preference, CPP-reinstatement, and rewarding effects of cocaine in the mesolimbic dopaminergic pathway.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCell LineCocaineConditioning, OperantDopamine Uptake InhibitorsDoxycyclineExtinction, PsychologicalImmunohistochemistryLentivirusMaleMotor ActivityNucleus AccumbensRatsRats, WistarReceptor, trkBBrain-Derived Neurotrophic FactorCocaineDopamine Uptake InhibitorsDoxycyclineReceptor, trkBRNA, Small Interfering

Identifiers

PMID18551281
OpenAlexW2060476762

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.