Evidence map›Paper›PMID 26188600›Full record

ArticleBiological psychiatry2016

Mice Lacking GPR88 Show Motor Deficit, Improved Spatial Learning, and Low Anxiety Reversed by Delta Opioid Antagonist.

Aura C Meirsman, Julie Le Merrer, Lucie P Pellissier, Jorge Diaz, Daniel Clesse, Brigitte L Kieffer, Jérôme A J Becker

Abstract read
In one paragraph

Article in Biological psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 86 citations in OpenAlex.

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  15. Striatal Cholinergic Interneurons Are Required for Contending Strategy Selection While Solving Spatial Navigation Problems.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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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

7 authors at 6 institutions in 2 countries.

Aura C MeirsmanDépartement de Médecine Translationnelle et Neurogénétique, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut National de la Santé et de la Recherche Médicale U-964, National de la Recherche Scientifique UMR-7104, Université de Strasbourg, Illkirch, France.
Julie Le MerrerDépartement de Médecine Translationnelle et Neurogénétique, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut National de la Santé et de la Recherche Médicale U-964, National de la Recherche Scientifique UMR-7104, Université de Strasbourg, Illkirch, France.; Physiologie de la Reproduction et des Comportements, Institut National de la Recherche Agronomique UMR-0085, National de la Recherche Scientifique UMR-7247, Université François Rabelais de Tours, Nouzilly, France.
Lucie P PellissierPhysiologie de la Reproduction et des Comportements, Institut National de la Recherche Agronomique UMR-0085, National de la Recherche Scientifique UMR-7247, Université François Rabelais de Tours, Nouzilly, France.
Jorge DiazCentre de Psychiatrie et Neurosciences, Institut National de la Santé et de la Recherche Médicale UMR-894 - Université Paris Descartes, Paris, France.
Daniel ClesseDépartement de Neurobiologie des rythmes, Institut des Neurosciences Cellulaires et Intégratives, National de la Recherche Scientifique UPR-3212, Université de Strasbourg, Strasbourg, France.
Brigitte L KiefferDépartement de Médecine Translationnelle et Neurogénétique, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut National de la Santé et de la Recherche Médicale U-964, National de la Recherche Scientifique UMR-7104, Université de Strasbourg, Illkirch, France.. Electronic address: Brigitte.Kieffer@douglas.mcgill.ca.
Jérôme A J BeckerDépartement de Médecine Translationnelle et Neurogénétique, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Institut National de la Santé et de la Recherche Médicale U-964, National de la Recherche Scientifique UMR-7104, Université de Strasbourg, Illkirch, France.; Physiologie de la Reproduction et des Comportements, Institut National de la Recherche Agronomique UMR-0085, National de la Recherche Scientifique UMR-7247, Université François Rabelais de Tours, Nouzilly, France.
Institut de génétique et de biologie moléculaire et cellulaire · FRInstitut des Neurosciences Cellulaires et Intégratives · FRMaison Interuniversitaire des Sciences de l'Homme · FRPhysiologie de la Reproduction et des Comportements · FRUniversité de Strasbourg · FRUniversité Paris Cité · FR

Funding

The Role of Striosome Neurons in Mediating Opiod RewardP50DA005010 · NIDA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIANGDONG WILLIAM · 1987 to 2021
$30.7M
Nr4a1 and GPR88 as novel gene targets for alcoholism: mouse genetic approachesU01AA016658 · NIAAA · UNIVERSITE DE STRASBOURG · PI LAURA ADELA HARSAN · 2006 to 2026
$3.8M
NIAAA NIH HHS U01 AA016658NIDA NIH HHS P50 DA005010
6 · The paper itself

Abstract

backgroundGPR88 is an orphan G protein coupled receptor highly enriched in the striatum, and previous studies have focused on GPR88 function in striatal physiology. The receptor is also expressed in other brain areas, and here we examined whether GPR88 function extends beyond striatal-mediated responses.

methodsWe created Gpr88 knockout mice and examined both striatal and extrastriatal regions at molecular and cellular levels. We also tested striatum-, hippocampus-, and amygdala-dependent behaviors in Gpr88(-/-) mice using extensive behavioral testing.

resultsWe found increased G protein coupling for delta opioid receptor (DOR) and mu opioid, but not other Gi/o coupled receptors, in the striatum of Gpr88 knockout mice. We also found modifications in gene transcription, dopamine and serotonin contents, and dendritic morphology inside and outside the striatum. Behavioral testing confirmed striatal deficits (hyperactivity, stereotypies, motor impairment in rotarod). In addition, mutant mice performed better in spatial tasks dependent on hippocampus (Y-maze, novel object recognition, dual solution cross-maze) and also showed markedly reduced levels of anxiety (elevated plus maze, marble burying, novelty suppressed feeding). Strikingly, chronic blockade of DOR using naltrindole partially improved motor coordination and normalized spatial navigation and anxiety of Gpr88(-/-) mice.

conclusionsWe demonstrate that GPR88 is implicated in a large repertoire of behavioral responses that engage motor activity, spatial learning, and emotional processing. Our data also reveal functional antagonism between GPR88 and DOR activities in vivo. The therapeutic potential of GPR88 therefore extends to cognitive and anxiety disorders, possibly in interaction with other receptor systems.

Indexed as

AmygdalaAnimalsAnxietyCorpus StriatumDendritesDopamineFemaleHippocampusMaleMice, Inbred C57BLMice, KnockoutMovement DisordersNaltrexoneNarcotic AntagonistsReceptors, G-Protein-CoupledReceptors, Opioid, deltaDopamineGpr88 protein, mouseNaltrexonenaltrindoleNarcotic AntagonistsReceptors, G-Protein-CoupledReceptors, Opioid, deltaReceptors, Opioid, muSerotoninEthological scoring of anxietyGene clusteringGPR88 agonist-induced GTPγS bindingMedium spiny neuronsPsychiatric disordersSpatial learning

Identifiers

PMID26188600
PMCPMC4670823
OpenAlexW647659435

What OpenQuestion holds

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Registered trials

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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.