ArticleBritish journal of pharmacology2012
The orphan receptor GPR3 modulates the early phases of cocaine reinforcement.
Article in British journal of pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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.
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.
Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Schizophrenia: from mechanism to therapy.Science China. Life sciences · 2026Review
- Discovery of Small Molecule Ligands Targeting Orphan G Protein-Coupled Receptors GPR3, GPR6, and GPR12.Journal of medicinal chemistry · 2026Review
- Targeting GPR3 as a novel approach for nicotine cessation therapeutic development.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Beyond the hype: a comprehensive exploration of CBD's biological impacts and mechanisms of action.Journal of cannabis research · 2025Review
- Lipid-Dependent Activation of the Orphan G Protein-Coupled Receptor, GPR3.Biochemistry · 2024Article
- Identification of oleic acid as an endogenous ligand of GPR3.Cell research · 2024Article
- The development of diphenyleneiodonium analogs as GPR3 agonists.Bioorganic & medicinal chemistry letters · 2023Article
- G protein-biased GPR3 signaling ameliorates amyloid pathology in a preclinical Alzheimer's disease mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Advances in Neurobiology and Pharmacology of GPR12.Frontiers in pharmacology · 2020Review
- Cannabidiol Treatment Might Promote Resilience to Cocaine and Methamphetamine Use Disorders: A Review of Possible Mechanisms.Molecules (Basel, Switzerland) · 2019Review
- GPR3, GPR6, and GPR12 as novel molecular targets: their biological functions and interaction with cannabidiol.Acta pharmacologica Sinica · 2019Review
- Allosteric sodium binding cavity in GPR3: a novel player in modulation of Aβ production.Scientific reports · 2018Article
- Towards a better understanding of the cannabinoid-related orphan receptors GPR3, GPR6, and GPR12.Drug metabolism reviews · 2018Review
- A Brain-Region-Specific Neural Pathway Regulating Germinal Matrix Angiogenesis.Developmental cell · 2017Article
- Exposure of adolescent mice to 3,4-methylenedioxypyrovalerone increases the psychostimulant, rewarding and reinforcing effects of cocaine in adulthood.British journal of pharmacology · 2017Article
- Neuro-psychopharmacological perspective of Orphan receptors of Rhodopsin (class A) family of G protein-coupled receptors.Psychopharmacology · 2017Review
- Methods for the Development of In Silico GPCR Models.Methods in enzymology · 2017Article
- An Update on Non-CBCannabis and cannabinoid research · 2017Review
- Maternal Separation Impairs Cocaine-Induced Behavioural Sensitization in Adolescent Mice.PloS one · 2016Article
- The Subcellular Dynamics of the Gs-Linked Receptor GPR3 Contribute to the Local Activation of PKA in Cerebellar Granular Neurons.PloS one · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeThe modulatory activity of the orphan receptor GPR3 in the brain has been related to the control of emotional behaviours. Limbic structures that express GPR3 have been associated with the effects of drug abuse. EXPERIMENTAL APPROACH: The role of GPR3 in different cocaine-elicited behaviours including locomotor activity, behavioural sensitization, conditioned place preference (CPP) and intravenous self-administration was evaluated in Gpr3-/- mice and their Gpr3+/+ littermates. Cocaine-induced dopamine release in the nucleus accumbens was also evaluated to elucidate the effect of Gpr3 deletion on extracellular levels of dopamine. KEY
resultsGpr3-/- mice exhibited higher rewarding responses in the CPP paradigm. Gpr3-/- mice self-administered more cocaine, especially during the first days of training. No differences were found between genotypes regarding behavioural sensitization and the maximal effort required to obtain a cocaine infusion. Non-contingent priming injections of cocaine before operant training eliminated enhanced cocaine self-administration in Gpr3-/- mice. Extracellular levels of dopamine in the nucleus accumbens induced by cocaine did not differ between genotypes. CONCLUSIONS AND IMPLICATIONS: The increased responsiveness of Gpr3-/- mice to the acute locomotor effects of cocaine and the inconsistency to further increase this effect reflected an 'already maximally sensitized' basal state. Enhanced responsiveness of Gpr3-/- mice to cocaine reward and to early phases of reinforcement suggests that an initial alteration increased vulnerability to this type of drug abuse. Overall, altered signalling pathways of GPR3 could contribute to the neurobiological substrate involved in developing addiction to cocaine.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.