ArticleNature neuroscience2012
Lack of GPR88 enhances medium spiny neuron activity and alters motor- and cue-dependent behaviors.
Article in Nature neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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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.
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Who cites it
79 citing papers in PubMed, 116 citations in OpenAlex.
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- STELLA: a spatial transcriptomics framework for microenvironment decoding using dynamic graph neural networks.Science China. Life sciences · 2026Article
- GPR88 localization to primary cilia in neurons is cell-type specific.Life science alliance · 2026Article
- Orphan G Protein-Coupled Receptor GPR88: Mapping Its Significance in Central Nervous System Disorders.Molecular neurobiology · 2025Review
- Bmal1 Modulates Striatal cAMP Signaling and Motor Learning.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Identifying disease progression biomarkers in metabolic associated steatotic liver disease (MASLD) through weighted gene co-expression network analysis and machine learning.Journal of translational medicine · 2025Article
- Maximising translational value of the Iowa gambling task in preclinical studies through the use of the rodent touchscreen.Frontiers in psychiatry · 2025Review
- The GPR88 Agonist RTI-122 Reduces Alcohol-Related Motivation and Consumption.Addiction biology · 2025Article
- GPR88 promotes neurite outgrowth of sensory neurons via activation of GFrontiers in pharmacology · 2025Article
- Orphan GPCRs in Neurodegenerative Disorders: Integrating Structural Biology and Drug Discovery Approaches.Current issues in molecular biology · 2024Review
- Orphan peptide and G protein-coupled receptor signalling in alcohol use disorder.British journal of pharmacology · 2024Review
- Design, Synthesis, and Structure-Activity Relationship Studies of Novel GPR88 Agonists (4-Substituted-phenyl)acetamides Based on the Reversed Amide Scaffold.ACS chemical neuroscience · 2024Article
- Article
- Neonatal immune challenge poses a sex-specific risk for epigenetic microglial reprogramming and behavioral impairment.Nature communications · 2023Article
- Synthesis and pharmacological validation of a novel radioligand for the orphan GPR88 receptor.Bioorganic & medicinal chemistry letters · 2023Article
- The cortico-striatal circuitry in autism-spectrum disorders: a balancing act.Frontiers in cellular neuroscience · 2023Review
- The orphan receptor GPR88 controls impulsivity and is a risk factor for Attention-Deficit/Hyperactivity Disorder.Molecular psychiatry · 2022Article
- The GPR88 agonist RTI-13951-33 reduces alcohol drinking and seeking in mice.Addiction biology · 2022Article
- Activation and allosteric regulation of the orphan GPR88-Gi1 signaling complex.Nature communications · 2022Article
- Update on GPCR-based targets for the development of novel antidepressants.Molecular psychiatry · 2022Review
19 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
The striatum regulates motor control, reward and learning. Abnormal function of striatal GABAergic medium spiny neurons (MSNs) is believed to contribute to the deficits in these processes that are observed in many neuropsychiatric diseases. The orphan G protein-coupled receptor GPR88 is robustly expressed in MSNs and is regulated by neuropharmacological drugs, but its contribution to MSN physiology and behavior is unclear. We found that, in the absence of GPR88, MSNs showed increased glutamatergic excitation and reduced GABAergic inhibition, which promoted enhanced firing rates in vivo, resulting in hyperactivity, poor motor coordination and impaired cue-based learning in mice. Targeted viral expression of GPR88 in MSNs rescued the molecular and electrophysiological properties and normalized behavior, suggesting that aberrant MSN activation in the absence of GPR88 underlies behavioral deficits and its dysfunction may contribute to behaviors observed in neuropsychiatric disease.
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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.