Evidence map›Paper›PMID 33257326›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2021

CB1 Receptor Signaling Modulates Amygdalar Plasticity during Context-Cocaine Memory Reconsolidation to Promote Subsequent Cocaine Seeking.

Jessica A Higginbotham, Rong Wang, Ben D Richardson, Hiroko Shiina, Shi Min Tan, Mark A Presker, David J Rossi, Rita A Fuchs

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
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  4. Dorsal raphe to basolateral amygdala corticotropin-releasing factor circuit regulates cocaine-memory reconsolidation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  5. Article
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  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
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  13. A role for amygdala endocannabinoid signaling in reconsolidation of cocaine-associated memories.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  14. 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

8 authors at 3 institutions in 1 country.

Jessica A HigginbothamDepartment of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, Washington 99164.ORCID 0000-0001-7360-8971
Rong WangDepartment of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, Washington 99164.
Ben D RichardsonDepartment of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, Washington 99164.ORCID 0000-0003-0403-4956
Hiroko ShiinaDepartment of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, Washington 99164.ORCID 0000-0003-4016-2285
Shi Min TanDepartment of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, Washington 99164.
Mark A PreskerDepartment of Psychology and Neuroscience, University of North Carolina, Chapel Hill, North Carolina 27599.
David J RossiDepartment of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, Washington 99164.ORCID 0000-0002-6703-0330
Rita A FuchsDepartment of Integrative Physiology and Neuroscience, Washington State University College of Veterinary Medicine, Pullman, Washington 99164 rita.fuchs@wsu.edu.ORCID 0000-0002-5999-9969
Washington State University · USUniversity of Idaho · USUniversity of North Carolina at Chapel Hill · US

Funding

RESEARCH TRAINING IN THE NEUROSCIENCEST32NS007431 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Juan Song, Mark J. Zylka · 1997 to 2026
$10.0M
Drug Context-Induced Instrumental Cocaine Seeking: Influence of Memory ReconsolidR01DA025646 · NIDA · WASHINGTON STATE UNIVERSITY · PI FUCHS LOKENSGARD, RITA A · 2010 to 2021
$3.5M
Cerebellar Contributions to Alcohol Use DisordersR01AA026078 · NIAAA · WASHINGTON STATE UNIVERSITY · PI ROSSI, DAVID J · 2017 to 2021
$1.7M
Regulatory mechanisms of cocaine memory reconsolidation in the basolateral amygdalaF31DA045430 · NIDA · WASHINGTON STATE UNIVERSITY · PI HIGGINBOTHAM, JESSICA · 2018 to 2019
$45k
NIAAA NIH HHS R01 AA026078NIDA NIH HHS F31 DA045430NIDA NIH HHS R01 DA025646NINDS NIH HHS T32 NS007431
6 · The paper itself

Abstract

Contextual drug-associated memories precipitate craving and relapse in cocaine users. Such associative memories can be weakened through interference with memory reconsolidation, a process by which memories are maintained following memory retrieval-induced destabilization. We hypothesized that cocaine-memory reconsolidation requires cannabinoid type 1 receptor (CB1R) signaling based on the fundamental role of the endocannabinoid system in synaptic plasticity and emotional memory processing. Using an instrumental model of cocaine relapse, we evaluated whether systemic CB1R antagonism (AM251; 3 mg/kg, i.p.) during memory reconsolidation altered (1) subsequent drug context-induced cocaine-seeking behavior as well as (2) cellular adaptations and (3) excitatory synaptic physiology in the basolateral amygdala (BLA) in male Sprague Dawley rats. Systemic CB1R antagonism, during, but not after, cocaine-memory reconsolidation reduced drug context-induced cocaine-seeking behavior 3 d, but not three weeks, later. CB1R antagonism also inhibited memory retrieval-associated increases in BLA zinc finger 268 (zif268) and activity regulated cytoskeletal-associated protein (Arc) immediate-early gene (IEG) expression and changes in BLA AMPA receptor (AMPAR) and NMDA receptor (NMDAR) subunit phosphorylation that likely contribute to increased receptor membrane trafficking and synaptic plasticity during memory reconsolidation. Furthermore, CB1R antagonism increased memory reconsolidation-associated spontaneous EPSC (sEPSC) frequency in BLA principal neurons during memory reconsolidation. Together, these findings suggest that CB1R signaling modulates cellular and synaptic mechanisms in the BLA that may facilitate cocaine-memory strength by enhancing reconsolidation or synaptic reentry reinforcement, or by inhibiting extinction-memory consolidation. These findings identify the CB1R as a potential therapeutic target for relapse prevention.

Indexed as

AmygdalaAnimalsCocaineCocaine-Related DisordersDrug-Seeking BehaviorEndocannabinoidsExcitatory Postsynaptic PotentialsExtinction, PsychologicalGene Expression RegulationMaleMemory ConsolidationNeuronal PlasticityRatsRats, Sprague-DawleyReceptor, Cannabinoid, CB1Self AdministrationCocaineEndocannabinoidsReceptor, Cannabinoid, CB1amygdalaCB1cocaineendocannabinoidmemory reconsolidationreinstatement

Identifiers

PMID33257326
PMCPMC7842758
OpenAlexW3107840199

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.