Evidence map›Paper›PMID 28315693›Full record

ArticlePhysiology & behavior2017

Central GLP-1 receptor activation modulates cocaine-evoked phasic dopamine signaling in the nucleus accumbens core.

Samantha M Fortin, Mitchell F Roitman

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Physiology & behavior, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
3.2field-weighted citation impact, top 7% 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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
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  13. GLP-1 Receptor Agonists and Research to Treat Overeating and Substance Use Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Review
  14. Review
  15. Article
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  18. Effects of GLP-1 Receptor Agonists in Alcohol Use Disorder.Basic & clinical pharmacology & toxicology · 2025
    Review
  19. 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

2 authors at 1 institution in 1 country.

Samantha M FortinGraduate Program in Neuroscience, University of Illinois at Chicago, 840 South Wood Street, Chicago, IL 60612, USA. Electronic address: sforti2@uic.edu.
Mitchell F RoitmanGraduate Program in Neuroscience, University of Illinois at Chicago, 840 South Wood Street, Chicago, IL 60612, USA; Department of Psychology, University of Illinois at Chicago, 1007 W Harrison St, Chicago, IL 60607, USA. Electronic address: mroitman@uic.edu.
University of Illinois Chicago · US

Funding

Modulation of NAc-DA Signaling by Learning Motivational State and PeptidesR01DA025634 · NIDA · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ROITMAN, MITCHELL F · 2009 to 2024
$5.1M
NIDA NIH HHS R01 DA025634
6 · The paper itself

Abstract

Drugs of abuse increase the frequency and magnitude of brief (1-3s), high concentration (phasic) dopamine release events in terminal regions. These are thought to be a critical part of drug reinforcement and ultimately the development of addiction. Recently, metabolic regulatory peptides, including the satiety signal glucagon-like peptide-1 (GLP-1), have been shown to modulate cocaine reward-driven behavior and sustained dopamine levels after cocaine administration. Here, we use fast-scan cyclic voltammetry (FSCV) to explore GLP-1 receptor (GLP-1R) modulation of dynamic dopamine release in the nucleus accumbens (NAc) during cocaine administration. We analyzed dopamine release events in both the NAc shell and core, as these two subregions are differentially affected by cocaine and uniquely contribute to motivated behavior. We found that central delivery of the GLP-1R agonist Exendin-4 suppressed the induction of phasic dopamine release events by intravenous cocaine. This effect was selective for dopamine signaling in the NAc core. Suppression of phasic signaling in the core by Exendin-4 could not be attributed to interference with cocaine binding to one of its major substrates, the dopamine transporter, as cocaine-induced increases in reuptake were unaffected. The results suggest that GLP-1R activation, instead, exerts its suppressive effects by altering dopamine release - possibly by suppressing the excitability of dopamine neurons. Given the role of NAc core dopamine in the generation of conditioned responses based on associative learning, suppression of cocaine-induced dopamine signaling in this subregion by GLP-1R agonism may decrease the reinforcing properties of cocaine. Thus, GLP-1Rs remain viable targets for the treatment and prevention of cocaine seeking, taking and relapse.

Indexed as

Analysis of VarianceAnimalsCocaineDopamineDopamine Uptake InhibitorsElectrolysisExenatideGlucagon-Like Peptide-2 ReceptorHypoglycemic AgentsMaleNucleus AccumbensPeptidesRatsRats, Sprague-DawleySignal TransductionTime FactorsCocaineDopamineDopamine Uptake InhibitorsExenatideGlucagon-Like Peptide-2 ReceptorHypoglycemic AgentsPeptidesVenomsCocaineDopamineDrug addictionGlucagon-like peptide-1Nucleus accumbensReward

Identifiers

PMID28315693
PMCPMC5763906
OpenAlexW2596879656

What OpenQuestion holds

Textmetadata
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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.