Evidence map›Paper›PMID 26706696›Full record

ArticleEuropean neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology2016

Ceftriaxone attenuates cocaine relapse after abstinence through modulation of nucleus accumbens AMPA subunit expression.

Amber L LaCrosse, Kristine Hill, Lori A Knackstedt

Abstract read
In one paragraph

Article in European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

  1. The role of the prelimbic cortex to nucleus accumbens core projection in the reinstatement of cocaine-seeking after cocaine-alcohol polysubstance use.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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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

3 authors at 1 institution in 1 country.

Amber L LaCrossePsychology Department, University of Florida, Gainesville, FL, United States.
Kristine HillPsychology Department, University of Florida, Gainesville, FL, United States.
Lori A KnackstedtPsychology Department, University of Florida, Gainesville, FL, United States. Electronic address: knack@ufl.edu.
University of Florida · US

Funding

Glutamate Transporters and Cocaine SeekingR01DA033436 · NIDA · UNIVERSITY OF FLORIDA · PI KNACKSTEDT, LORI A · 2012 to 2016
$1.3M
NIDA NIH HHS DA033436NIDA NIH HHS R01 DA033436
6 · The paper itself

Abstract

Using the extinction-reinstatement model of cocaine relapse, we and others have demonstrated that the antibiotic ceftriaxone attenuates cue- and cocaine-primed reinstatement of cocaine-seeking. Reinstatement is contingent on the release of glutamate in the nucleus accumbens core (NAc) and manipulations that reduce glutamate efflux or block post-synaptic glutamate receptors attenuate reinstatement. We have demonstrated that the mechanism of action by which ceftriaxone attenuates reinstatement involves increased NAc GLT-1 expression and a reduction in NAc glutamate efflux during reinstatement. Here we investigated the effects of ceftriaxone (100 and 200 mg/kg) on context-primed relapse following abstinence without extinction training and examined the effects of ceftriaxone on GluA1, GluA2 and GLT-1 expression. We conducted microdialysis during relapse to determine if an increase in NAc glutamate accompanies relapse after abstinence and whether ceftriaxone blunts glutamate efflux. We found that both doses of ceftriaxone attenuated relapse. While relapse was accompanied by an increase in NAc glutamate, ceftriaxone (200 mg/kg) was unable to significantly reduce NAc glutamate efflux during relapse despite its ability to upregulate GLT-1. GluA1 was reduced in the NAc by both doses of ceftriaxone while GluA2 expression was unchanged, indicating that ceftriaxone altered AMPA subunit composition following cocaine. Finally, GLT-1 was not altered in the PFC by ceftriaxone. These results indicate that it is possible to attenuate context-primed relapse to cocaine-seeking through modification of post-synaptic receptor properties without attenuating glutamate efflux during relapse. Furthermore, increasing NAc GLT-1 protein expression is not sufficient to attenuate glutamate efflux.

Indexed as

Analysis of VarianceAnimalsAnti-Bacterial AgentsArea Under CurveCeftriaxoneChromatography, High Pressure LiquidCocaineCocaine-Related DisordersConditioning, OperantDose-Response Relationship, DrugExcitatory Amino Acid Transporter 2Gene Expression RegulationGlutamic AcidMaleNucleus AccumbensRatsAnti-Bacterial AgentsCeftriaxoneCocaineExcitatory Amino Acid Transporter 2Glutamic AcidReceptors, AMPASlc1a2 protein, ratCocaineGLT-1GluA1GlutamateNucleus accumbensRelapse

Identifiers

PMID26706696
PMCPMC4762719
OpenAlexW2189951856

What OpenQuestion holds

Textmetadata
LicenceTDM
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.