Evidence map›Paper›PMID 26612422›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2016

Differential Control of Cocaine Self-Administration by GABAergic and Glutamatergic CB1 Cannabinoid Receptors.

Elena Martín-García, Lucie Bourgoin, Adeline Cathala, Fernando Kasanetz, Miguel Mondesir, Ana Gutiérrez-Rodriguez, Leire Reguero, Jean-François Fiancette, Pedro Grandes, Umberto Spampinato and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Cannabinoid CB1 receptor and mu-opioid receptor interaction: new insights from conditional knockout mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  3. Role of mesolimbic cannabinoid receptor 1 in stress-driven increases in cocaine self-administration in male rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Article
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  19. 17β-Estradiol Potentiates the Reinstatement of Cocaine Seeking in Female Rats: Role of the Prelimbic Prefrontal Cortex and Cannabinoid Type-1 Receptors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  20. Preclinical Studies of Cannabinoid Reward, Treatments for Cannabis Use Disorder, and Addiction-Related Effects of Cannabinoid Exposure.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Elena Martín-GarcíaINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Lucie BourgoinINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Adeline CathalaINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Fernando KasanetzINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.ORCID 0000-0003-4585-2314
Miguel MondesirINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Ana Gutiérrez-RodriguezDepartment of Neurosciences, Faculty of Medicine and Dentistry, University of the Basque Country UPV/EHU, Leioa, Spain.
Leire RegueroDepartment of Neurosciences, Faculty of Medicine and Dentistry, University of the Basque Country UPV/EHU, Leioa, Spain.
Jean-François FiancetteINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Pedro GrandesDepartment of Neurosciences, Faculty of Medicine and Dentistry, University of the Basque Country UPV/EHU, Leioa, Spain.
Umberto SpampinatoINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Rafael MaldonadoDepartament de Ciencies Experimentals i de la Salut, Universitat Pompeu Fabra, PRBB, Barcelona, Spain.
Pier Vincenzo PiazzaINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Giovanni MarsicanoUniversity of Bordeaux, Bordeaux, France.
Véronique Deroche-GamonetINSERM U862, Pathophysiology of Addiction, NeuroCentre Magendie, Bordeaux, France.
Université de Bordeaux · FRUniversity of the Basque Country · ESUniversitat Pompeu Fabra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The type 1 cannabinoid receptor (CB1) modulates numerous neurobehavioral processes and is therefore explored as a target for the treatment of several mental and neurological diseases. However, previous studies have investigated CB1 by targeting it globally, regardless of its two main neuronal localizations on glutamatergic and GABAergic neurons. In the context of cocaine addiction this lack of selectivity is critical since glutamatergic and GABAergic neuronal transmission is involved in different aspects of the disease. To determine whether CB1 exerts different control on cocaine seeking according to its two main neuronal localizations, we used mutant mice with deleted CB1 in cortical glutamatergic neurons (Glu-CB1) or in forebrain GABAergic neurons (GABA-CB1). In Glu-CB1, gene deletion concerns the dorsal telencephalon, including neocortex, paleocortex, archicortex, hippocampal formation and the cortical portions of the amygdala. In GABA-CB1, it concerns several cortical and non-cortical areas including the dorsal striatum, nucleus accumbens, thalamic, and hypothalamic nuclei. We tested complementary components of cocaine self-administration, separating the influence of primary and conditioned effects. Mechanisms underlying each phenotype were explored using in vivo microdialysis and ex vivo electrophysiology. We show that CB1 expression in forebrain GABAergic neurons controls mouse sensitivity to cocaine, while CB1 expression in cortical glutamatergic neurons controls associative learning processes. In accordance, in the nucleus accumbens, GABA-CB1 receptors control cocaine-induced dopamine release and Glu-CB1 receptors control AMPAR/NMDAR ratio; a marker of synaptic plasticity. Our findings demonstrate a critical distinction of the altered balance of Glu-CB1 and GABA-CB1 activity that could participate in the vulnerability to cocaine abuse and addiction. Moreover, these novel insights advance our understanding of CB1 neuropathophysiology.

Indexed as

Drug-Seeking BehaviorAnimalsBrainCocaineCuesDopamineGABAergic NeuronsGlutamic AcidMiceMice, KnockoutNeuronsNucleus AccumbensReceptor, Cannabinoid, CB1Receptors, AMPAReceptors, N-Methyl-D-AspartateReinforcement, PsychologyCocaineDopamineGlutamic AcidReceptor, Cannabinoid, CB1Receptors, AMPAReceptors, N-Methyl-D-Aspartate

Identifiers

PMID26612422
PMCPMC4946049
OpenAlexW2172876381

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.