Evidence map›Paper›PMID 24442095›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014

Dopamine in the dorsal hippocampus impairs the late consolidation of cocaine-associated memory.

Cecilia P Kramar, Vladimir I Chefer, Roy A Wise, Jorge H Medina, M Flavia Barbano

Abstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. A Critical Time Window of Neocortex Modulation for Remote Fear Memory in Rats and Humans.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  2. Article
  3. What could evolve in the evolution of memory?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  4. Article
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  6. Review
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  12. Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020
    Review
  13. Article
  14. Article
  15. Article
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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

5 authors.

Cecilia P KramarInstituto de Biología Celular y Neurociencias (CONICET-UBA), Facultad de Medicina, UBA, Buenos Aires, Argentina.
Vladimir I CheferNational Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD, USA.
Roy A WiseNational Institute on Drug Abuse, Intramural Research Program, National Institutes of Health, Baltimore, MD, USA.
Jorge H Medina1] Instituto de Biología Celular y Neurociencias (CONICET-UBA), Facultad de Medicina, UBA, Buenos Aires, Argentina [2] Departamento de Fisiología, Facultad de Medicina, UBA, Buenos Aires, Argentina.
M Flavia BarbanoInstituto de Biología Celular y Neurociencias (CONICET-UBA), Facultad de Medicina, UBA, Buenos Aires, Argentina.

Funding

Microdialysis Studies of Self-administrationxZIADA000471 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI WISE, ROY A · 2009 to 2018
$16.4M
Intramural NIH HHS Z99 DA999999
6 · The paper itself

Abstract

Cocaine is thought to be addictive because it elevates dopamine levels in the striatum, reinforcing drug-seeking habits. Cocaine also elevates dopamine levels in the hippocampus, a structure involved in contextual conditioning as well as in reward function. Hippocampal dopamine promotes the late phase of consolidation of an aversive step-down avoidance memory. Here, we examined the role of hippocampal dopamine function in the persistence of the conditioned increase in preference for a cocaine-associated compartment. Blocking dorsal hippocampal D1-type receptors (D1Rs) but not D2-type receptors (D2Rs) 12 h after a single training trial extended persistence of the normally short-lived memory; conversely, a general and a specific phospholipase C-coupled D1R agonist (but not a D2R or adenylyl cyclase-coupled D1R agonist) decreased the persistence of the normally long-lived memory established by three-trial training. These effects of D1 agents were opposite to those previously established in a step-down avoidance task, and were here also found to be opposite to those in a lithium chloride-conditioned avoidance task. After returning to normal following cocaine injection, dopamine levels in the dorsal hippocampus were found elevated again at the time when dopamine antagonists and agonists were effective: between 13 and 17 h after cocaine injection. These findings confirm that, long after the making of a cocaine-place association, hippocampal activity modulates memory consolidation for that association via a dopamine-dependent mechanism. They suggest a dynamic role for dorsal hippocampal dopamine in this late-phase memory consolidation and, unexpectedly, differential roles for late consolidation of memories for places that induce approach or withdrawal because of a drug association.

Indexed as

AnimalsAssociation LearningBrain-Derived Neurotrophic FactorCocaineConditioning, OperantDisease Models, AnimalDopamineDopamine AgentsDopamine Uptake InhibitorsDose-Response Relationship, DrugDrug Administration RoutesHippocampusLithium ChlorideMaleMAP Kinase Signaling SystemMemory DisordersBrain-Derived Neurotrophic FactorCocaineDopamineDopamine AgentsDopamine Uptake InhibitorsLithium ChlorideReceptor, trkB

Identifiers

PMID24442095
PMCPMC4023137

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.