Evidence map›Paper›PMID 23303053›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013

A critical role for protein degradation in the nucleus accumbens core in cocaine reward memory.

Zhen-Yu Ren, Meng-Meng Liu, Yan-Xue Xue, Zeng-Bo Ding, Li-Fen Xue, Suo-Di Zhai, Lin Lu

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.1field-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

43 citing papers in PubMed, 73 citations in OpenAlex.

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  14. Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020
    Review
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  16. Article
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  19. Genome-wide transcriptional profiling of central amygdala and orbitofrontal cortex during incubation of methamphetamine craving.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  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

7 authors at 3 institutions in 1 country.

Zhen-Yu RenPharmacy Department, Peking University Third Hospital, Beijing, China.
Meng-Meng Liu
Yan-Xue Xue
Zeng-Bo Ding
Li-Fen Xue
Suo-Di Zhai
Lin Lu
Peking University · CNNational Institutes for Food and Drug Control · CNPeking University Third Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intense associative memories that develop between cocaine-paired contexts and rewarding stimuli contribute to cocaine seeking and relapse. Previous studies have shown impairment in cocaine reward memories by manipulating a labile state induced by memory retrieval, but the mechanisms that underlie the destabilization of cocaine reward memory are unknown. In this study, using a Pavlovian cocaine-induced conditioned place preference (CPP) procedure in rats, we tested the contribution of ubiquitin-proteasome system-dependent protein degradation in destabilization of cocaine reward memory. First, we found that polyubiquitinated protein expression levels and polyubiquitinated N-ethylmaleimide-sensitive fusion (NSF) markedly increased 15 min after retrieval while NSF protein levels decreased 1 h after retrieval in the synaptosomal membrane fraction in the nucleus accumbens (NAc) core. We then found that infusion of the proteasome inhibitor lactacystin into the NAc core prevented the impairment of memory reconsolidation induced by the protein synthesis inhibitor anisomycin and reversed the effects of anisomycin on NSF and glutamate receptor 2 (GluR2) protein levels in the synaptosomal membrane fraction in the NAc core. We also found that lactacystin infusion into the NAc core but not into the shell immediately after extinction training sessions inhibited CPP extinction and reversed the extinction training-induced decrease in NSF and GluR2 in the synaptosomal membrane fraction in the NAc core. Finally, infusions of lactacystin by itself into the NAc core immediately after each training session or before the CPP retrieval test had no effect on the consolidation and retrieval of cocaine reward memory. These findings suggest that ubiquitin-proteasome system-dependent protein degradation is critical for retrieval-induced memory destabilization.

Indexed as

ProteolysisRewardAnalysis of VarianceAnimalsCocaineConditioning, OperantDopamine Uptake InhibitorsEnzyme InhibitorsExtinction, PsychologicalMaleMemoryNucleus AccumbensPolyubiquitinRatsRats, Sprague-DawleyReceptors, AMPACocaineDopamine Uptake InhibitorsEnzyme Inhibitorsglutamate receptor ionotropic, AMPA 2PolyubiquitinReceptors, AMPAUbiquitin

Identifiers

PMID23303053
PMCPMC3672001
OpenAlexW2101667399

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.