Evidence map›Paper›PMID 26821978›Full record

ArticleMolecular psychiatry2016

Glutamatergic mechanisms of comorbidity between acute stress and cocaine self-administration.

C Garcia-Keller, Y M Kupchik, C D Gipson, R M Brown, S Spencer, F Bollati, M A Esparza, D J Roberts-Wolfe, J A Heinsbroek, A-C Bobadilla and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

32 citing papers in PubMed, 39 citations in OpenAlex.

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  13. Cannabinoid use is enhanced by stress and changes conditioned stress responses.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022
    Article
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  18. Behavioral and accumbens synaptic plasticity induced by cues associated with restraint stress.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  19. 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

12 authors at 4 institutions in 4 countries.

C Garcia-KellerDepartment of Neuroscience, Medical University of South Carolina, Charleston, SC, USA.
Y M KupchikDepartment of Medical Neurobiology, Institute for Medical Research Israel-Canada, Faculty of Medicine, The Hebrew University, Jerusalem, Israel.
C D GipsonDepartment of Neuroscience, Medical University of South Carolina, Charleston, SC, USA.
R M BrownFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia.
S SpencerDepartment of Neuroscience, Medical University of South Carolina, Charleston, SC, USA.ORCID 0000-0001-8663-9056
F BollatiIFEC-CONICET, Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
M A EsparzaIFEC-CONICET, Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
D J Roberts-WolfeDepartment of Neuroscience, Medical University of South Carolina, Charleston, SC, USA.
J A HeinsbroekDepartment of Neuroscience, Medical University of South Carolina, Charleston, SC, USA.
A-C BobadillaDepartment of Neuroscience, Medical University of South Carolina, Charleston, SC, USA.
L M CancelaIFEC-CONICET, Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba, Córdoba, Argentina.
P W KalivasDepartment of Neuroscience, Medical University of South Carolina, Charleston, SC, USA.
Medical University of South Carolina · USConsejo Nacional de Investigaciones Científicas y Técnicas · ARHebrew University of Jerusalem · ILThe University of Melbourne · AU

Funding

South Carolina Clinical & Translational Research Institute (SCTR)UL1TR001450 · NCATS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI BRADY, KATHLEEN T., FLUME, PATRICK A · 2015 to 2024
$41.1M
Selective Restoration of KCNQ Channel Inhibition in the PFC to Inhibit Cue-InducP50DA015369 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ASTON-JONES, GARY S. · 2003 to 2017
$18.6M
TRAINING PROGRAM FOR MEDICAL SCIENTISTST32GM008716 · NIGMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DEMORE, NANCY · 1999 to 2024
$9.3M
GLUTAMATE AND CRAVING FOR COCAINER01DA012513 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KALIVAS, PETER W · 2000 to 2024
$7.5M
OPIOIDS, AMPHETAMINE &COCAIN IN DRUG ABUSER01DA003906 · NIDA · WASHINGTON STATE UNIVERSITY · PI KALIVAS, PETER W · 1985 to 2019
$3.6M
Contributions of Glial Glutamate Transport and NMDA Receptors in Nicotine RelapseK99DA036569 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI GIPSON-REICHARDT, CASSANDRA D · 2014 to 2015
$262k
The Role of Transient Corticostriatal Synaptic Plasticity in Extinction from CocaineF30DA038893 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI ROBERTS-WOLFE, DOUGLAS J · 2015 to 2018
$147k
NCATS NIH HHS UL1 TR001450NIDA NIH HHS F30 DA038893NIDA NIH HHS K99 DA036569NIDA NIH HHS P50 DA015369NIDA NIH HHS R01 DA003906NIDA NIH HHS R01 DA012513NIGMS NIH HHS T32 GM008716
6 · The paper itself

Abstract

There is substantial comorbidity between stress disorders and substance use disorders (SUDs), and acute stress augments the locomotor stimulant effect of cocaine in animal models. Here we endeavor to understand the neural underpinnings of comorbid stress disorders and drug use by determining whether the glutamatergic neuroadaptations that characterize cocaine self-administration are induced by acute stress. Rats were exposed to acute (2 h) immobilization stress, and 3 weeks later the nucleus accumbens core was examined for changes in glutamate transport, glutamate-mediated synaptic currents and dendritic spine morphology. We also determined whether acute stress potentiated the acquisition of cocaine self-administration. Acute stress produced an enduring reduction in glutamate transport and potentiated excitatory synapses on medium spiny neurons. Acute stress also augmented the acquisition of cocaine self-administration. Importantly, by restoring glutamate transport in the accumbens core with ceftriaxone the capacity of acute stress to augment the acquisition of cocaine self-administration was abolished. Similarly, ceftriaxone treatment prevented stress-induced potentiation of cocaine-induced locomotor activity. However, ceftriaxone did not reverse stress-induced synaptic potentiation, indicating that this effect of stress exposure did not underpin the increased acquisition of cocaine self-administration. Reversing acute stress-induced vulnerability to self-administer cocaine by normalizing glutamate transport poses a novel treatment possibility for reducing comorbid SUDs in stress disorders.

Indexed as

AnimalsCeftriaxoneCentral Nervous System StimulantsCocaineCocaine-Related DisordersComorbidityDendritic SpinesExcitatory Amino Acid AgentsExtinction, PsychologicalGlutamic AcidMaleNucleus AccumbensRatsRats, Sprague-DawleySelf AdministrationStress, PsychologicalCeftriaxoneCentral Nervous System StimulantsCocaineExcitatory Amino Acid AgentsGlutamic Acid

Identifiers

PMID26821978
PMCPMC4823171
OpenAlexW2280243664

What OpenQuestion holds

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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.