Evidence map›Paper›PMID 26784278›Full record

ArticleBritish journal of pharmacology2016

The metabotropic glutamate 5 receptor is necessary for extinction of cocaine-associated cues.

Christina J Perry, Felicia Reed, Isabel C Zbukvic, Jee Hyun Kim, Andrew J Lawrence

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. 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
1.7field-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

14 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  6. Molecular and circuit mechanisms regulating cocaine memory.Cellular and molecular life sciences : CMLS · 2020
    Review
  7. Article
  8. Context and topography determine the role of basolateral amygdala metabotropic glutamate receptor 5 in appetitive Pavlovian responding.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    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 at 2 institutions in 1 country.

Christina J PerryBehavioural Neuroscience Division, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC,, Australia.
Felicia ReedFlorey Department of Neuroscience and Mental Health, University of Melbourne, Melbourne, VIC, Australia.
Isabel C ZbukvicBehavioural Neuroscience Division, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC,, Australia.
Jee Hyun KimBehavioural Neuroscience Division, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC,, Australia.
Andrew J LawrenceBehavioural Neuroscience Division, The Florey Institute of Neuroscience and Mental Health, Parkville, VIC,, Australia.
Florey Institute of Neuroscience and Mental Health · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposeThere is currently no medication approved specifically to treat cocaine addiction. Behavioural interventions such as cue exposure therapy (CET) rely heavily on new learning. Antagonism of the metabotropic glutamate 5 (mGlu5 ) receptor has emerged as a potential treatment, by reducing the reinforcing properties of cocaine. However, mGlu5 receptor activity is necessary for learning; therefore, such agents could interfere with behavioural treatments. We used a novel rodent model of CET to test the effects of mGlu5 negative and positive allosteric modulators (NAM and PAM) on behavioural therapy. EXPERIMENTAL APPROACH: Rats were trained to press a lever for cocaine in the presence of a discrete cue [conditioned stimulus (CS)] and then extinguished in the absence of the CS. Following lever extinction, half the rats received CS extinction in the same chambers but with the levers withdrawn; the remaining rats received no CS extinction. Before this session, rats received a systemic administration of either vehicle or a mGlu5 NAM (MTEP, experiment 1) or PAM (CDPPB, experiment 2). Cue-induced reinstatement was tested in a drug-free session the following day. KEY

resultsAt reinstatement, rats that had received CS extinction showed reduced responding. This effect was attenuated by MTEP treatment before CS extinction. In contrast, administration of CDPPB (PAM) led to decreased reinstatement the following day, regardless of extinction condition. CONCLUSION AND IMPLICATIONS: These results suggest that mGlu5 receptor activity is both necessary and sufficient for efficient extinction of a cocaine-associated CS. Therefore, mGlu5 PAMs could enhance the efficacy of CET.

Indexed as

CuesAnimalsBenzamidesCocaineCocaine-Related DisordersConditioning, PsychologicalMalePyrazolesPyridinesRats, Sprague-DawleyReceptor, Metabotropic Glutamate 5Thiazoles3-((2-methyl-1,3-thiazol-4-yl)ethynyl)pyridine3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl)benzamideBenzamidesCocainePyrazolesPyridinesReceptor, Metabotropic Glutamate 5Thiazoles

Identifiers

PMID26784278
PMCPMC5341241
OpenAlexW2296695064

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.