ArticleCerebral cortex (New York, N.Y. : 1991)2017
Dopamine D3 Receptor Modulates l-DOPA-Induced Dyskinesia by Targeting D1 Receptor-Mediated Striatal Signaling.
Article in Cerebral cortex (New York, N.Y. : 1991), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- The Signaling and Pharmacology of the Dopamine D1 Receptor.Frontiers in cellular neuroscience · 2021Pooled it
- Mesdopetam for the Treatment of Levodopa Induced Dyskinesia in Parkinson's Disease: A Randomized Phase 2b Trial.Movement disorders clinical practice · 2025Trial
- Structure-guided discovery of non-catechol dopamine D1 receptor ligands with biased agonism and antagonism.The Journal of biological chemistry · 2026Article
- Tic-related behaviors in Celsr3 mutant mice are contributed by alterations of striatal DMolecular psychiatry · 2025Article
- Locomotor activity depends on β-arrestin recruitment by the dopamine DPharmacological research · 2025Article
- Dopamine Receptors in Restless Legs Syndrome and Augmentation: A Novel Perspective Focused on D1 and D3 Receptor Dynamics.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Neurophysiological Treatment Effects of Mesdopetam, Pimavanserin and Amantadine in a Rodent Model of Levodopa-Induced Dyskinesia.The European journal of neuroscience · 2025Article
- Modulation of DBiomedicines · 2024Article
- IRL790 modulated striatal D1 neurons synaptic plasticity ameliorating levodopa-induced dyskinesia in mouse.Frontiers in aging neuroscience · 2024Article
- Amphiregulin blockade decreases the levodopa-induced dyskinesia in a 6-hydroxydopamine Parkinson's disease mouse model.CNS neuroscience & therapeutics · 2023Article
- Astrocytes mediate long-lasting synaptic regulation of ventral tegmental area dopamine neurons.Nature neuroscience · 2022Article
- Pharmacological targeting of G protein-coupled receptor heteromers.Pharmacological research · 2022Article
- Article
- Neurobiological and Pharmacological Perspectives of D3 Receptors in Parkinson's Disease.Biomolecules · 2022Review
- Dopamine Receptors: Is It Possible to Become a Therapeutic Target for Depression?Frontiers in pharmacology · 2022Review
- Class A and C GPCR Dimers in Neurodegenerative Diseases.Current neuropharmacology · 2022Review
- Current Knowledge on the Background, Pathophysiology and Treatment of Levodopa-Induced Dyskinesia-Literature Review.Journal of clinical medicine · 2021Review
- Chirality of Novel Bitopic Agonists Determines Unique Pharmacology at the Dopamine D3 Receptor.Biomolecules · 2021Article
- Dopamine D3 Receptor Plasticity in Parkinson's Disease and L-DOPA-Induced Dyskinesia.Biomedicines · 2021Review
- Loss of Function in Dopamine D3 Receptor Attenuates Left Ventricular Cardiac Fibroblast Migration and ProliferationFrontiers in cardiovascular medicine · 2021Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The dopamine D3 receptor (D3R) belongs to the dopamine D2-like receptor family and is principally located in the ventral striatum. However, previous studies reported D3R overexpression in the dorsal striatum following l-DOPA treatment in parkinsonian animals. This fact has drawn attention in the importance of D3R in l-DOPA-induced dyskinesia (LID). Here, we used D3R knockout mice to assess the role of D3R in LID and rotational sensitization in the hemiparkinsonian model. Mice lacking D3R presented a reduction in dyskinesia without interfering with the antiparkinsonian l-DOPA effect and were accompanied by a reduction in the l-DOPA-induced rotations. Interestingly, deleting D3R attenuated important molecular markers in the D1R-neurons such as FosB, extracellular signal-regulated kinase, and histone-3 (H3)-activation. Colocalization studies in D1R-tomato and D2R-green fluorescent protein BAC-transgenic mice indicated that l-DOPA-induced D3R overexpression principally occurs in D1R-containing neurons although it is also present in the D2R-neurons. Moreover, D3R pharmacological blockade with PG01037 reduced dyskinesia and the molecular markers expressed in D1R-neurons. In addition, this antagonist further reduced dyskinetic symptoms in D1R heterozygous mice, indicating a direct interaction between D1R and D3R. Together, our results demonstrate that D3R modulates the development of dyskinesia by targeting D1R-mediated intracellular signaling and suggest that decreasing D3R activity may help to ameliorate LID.
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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.