ArticleMolecular psychiatry2020
Arrestin recruitment to dopamine D2 receptor mediates locomotion but not incentive motivation.
Article in Molecular psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Dopamine and Dopamine Receptors in Alzheimer's Disease: A Systematic Review and Network Meta-Analysis.Frontiers in aging neuroscience · 2019Pooled it
- G protein diffusion states reveal receptor binding dynamics at single-molecule scale.Cell chemical biology · 2026Article
- Dopamine D2 receptors bypass canonical signaling to directly tune NMDA receptor function and aversive learning.Science advances · 2026Article
- β-arrestin recruitment facilitates a direct association with G proteins.Nature communications · 2026Article
- Distance-related functional connectivity alterations in first-episode, drug-naïve major depressive disorder: a resting-state fMRI study with atlas-based neurotransmitter correlates.BMC psychiatry · 2026Article
- A structural overview of G-protein-coupled receptors in neurological disorders.Acta pharmacologica Sinica · 2026Review
- Local GPCR density tips the balance of μ-opioid receptor trafficking.bioRxiv : the preprint server for biology · 2026Article
- Lost in translation: why don't dopamine D2 antagonists cure addictions?Journal of psychiatry & neuroscience : JPN · 2026Article
- Brain region-specific dopamine receptor changes and astrocyte activation influence tau pathology through CDK5 in Alzheimer's disease models.Journal of Alzheimer's disease : JAD · 2025Article
- Apomorphine differentially engages the cAMP and β-arrestin signaling pathways relative to dopamine at human dopamine receptors.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Mice carrying the human dopamine D2 receptor pathogenic mutation p.Met374Arg exhibit hyperactivity and aberrant D2 receptor function.Molecular pharmacology · 2025Article
- Molecular mechanism of β-arrestin 2 interaction with phosphorylated intracellular loop 3 of dopamine receptor D2.Communications biology · 2025Article
- Discrete spatiotemporal encoding of striatal dopamine transmission.Science (New York, N.Y.) · 2025Article
- Development of Mutant MBiochemistry · 2025Article
- Ligand-Induced Biased Activation of GPCRs: Recent Advances and New Directions from In Silico Approaches.Molecules (Basel, Switzerland) · 2025Review
- Monoamine alterations in Alzheimer's disease and their implications in comorbid neuropsychiatric symptoms.GeroScience · 2025Review
- Behavioral alterations in antibiotic-treated mice associated with gut microbiota dysbiosis: insights from 16S rRNA and metabolomics.Frontiers in neuroscience · 2025Article
- A golden age of muscarinic acetylcholine receptor modulation in neurological diseases.Nature reviews. Drug discovery · 2024Review
- Biased Dopamine DBiomolecules & therapeutics · 2024Article
- Arrestin-3 Agonism at Dopamine DBiological psychiatry · 2023Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The dopamine (DA) D2 receptor (D2R) is an important target for the treatment of neuropsychiatric disorders such as schizophrenia and Parkinson's disease. However, the development of improved therapeutic strategies has been hampered by our incomplete understanding of this receptor's downstream signaling processes in vivo and how these relate to the desired and undesired effects of drugs. D2R is a G protein-coupled receptor (GPCR) that activates G protein-dependent as well as non-canonical arrestin-dependent signaling pathways. Whether these effector pathways act alone or in concert to facilitate specific D2R-dependent behaviors is unclear. Here, we report on the development of a D2R mutant that recruits arrestin but is devoid of G protein activity. When expressed virally in "indirect pathway" medium spiny neurons (iMSNs) in the ventral striatum of D2R knockout mice, this mutant restored basal locomotor activity and cocaine-induced locomotor activity in a manner indistinguishable from wild-type D2R, indicating that arrestin recruitment can drive locomotion in the absence of D2R-mediated G protein signaling. In contrast, incentive motivation was enhanced only by wild-type D2R, signifying a dissociation in the mechanisms that underlie distinct D2R-dependent behaviors, and opening the door to more targeted therapeutics.
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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.