ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Persistent increase in olfactory type G-protein alpha subunit levels may underlie D1 receptor functional hypersensitivity in Parkinson disease.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. 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.
- The Signaling and Pharmacology of the Dopamine D1 Receptor.Frontiers in cellular neuroscience · 2021Pooled it
- Trial
- Aberrant striatal firing mediates impulsive decision-making in a mouse model of Parkinson's disease.Brain : a journal of neurology · 2026Article
- Axon terminal hypertrophy of striatal projection neurons with levodopa-induced dyskinesia priming.Frontiers in neuroscience · 2023Article
- Discovery of levodopa-induced dyskinesia-associated genes using genomic studies in patients and Drosophila behavioral analyses.Communications biology · 2022Article
- Highlighting the Dystonic Phenotype Related to GNAO1.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Neurobiological and Pharmacological Perspectives of D3 Receptors in Parkinson's Disease.Biomolecules · 2022Review
- Cerebrospinal fluid biomarkers for assessing Huntington disease onset and severity.Brain communications · 2022Article
- Fusion with Promiscuous GαInternational journal of molecular sciences · 2021Article
- Article
- Involvement of Autophagy in Levodopa-Induced Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Article
- Dopamine D3 Receptor Plasticity in Parkinson's Disease and L-DOPA-Induced Dyskinesia.Biomedicines · 2021Review
- Effects of Aging on Levo-Dihydroxyphenylalanine- Induced Dyskinesia in a Rat Model of Parkinson's Disease.Frontiers in aging neuroscience · 2021Article
- Dopamine D1 receptor signalling in dyskinetic Parkinsonian rats revealed by fiber photometry using FRET-based biosensors.Scientific reports · 2020Article
- The interactions of dopamine and oxidative damage in the striatum of patients with neurodegenerative diseases.Journal of neurochemistry · 2020Article
- Gnal haploinsufficiency causes genomic instability and increased sensitivity to haloperidol.Experimental neurology · 2019Article
- Effects of histone acetyltransferase inhibitors on L-DOPA-induced dyskinesia in a murine model of Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2018Article
- Signal transduction in L-DOPA-induced dyskinesia: from receptor sensitization to abnormal gene expression.Journal of neural transmission (Vienna, Austria : 1996) · 2018Review
- Hyperactive Response of Direct Pathway Striatal Projection Neurons to L-dopa and D1 Agonism in Freely Moving Parkinsonian Mice.Frontiers in neural circuits · 2018Article
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Authors and funding
8 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Although L-dopa remains the most effective treatment of Parkinson disease, its long-term administration is hampered by the appearance of dyskinesia. Hypersensitivity of dopamine D1 receptors in the striatum has been suggested to contribute to the genesis of these delayed adverse effects. However, D1 receptor amounts are unchanged in Parkinson disease, suggesting alterations of downstream effectors. In rodents, striatal D1 receptors activate adenylyl cyclase through olfactory type G-protein alpha subunit (Galphaolf) and G-protein gamma 7 subunit (Ggamma7). We found that Galphaolf was enriched in human basal ganglia and was markedly diminished in the putamen of patients with Huntington disease, in relation with the degeneration of medium spiny neurons. In contrast, in the putamen of patients with Parkinson disease, Galphaolf and Ggamma7 levels were both significantly increased. In the rat, the degeneration of dopamine neurons augmented Galphaolf levels in the striatal neurons, specifically at the plasma membrane, an effect accounting for the increase of D1 response on cAMP production in dopamine-depleted striatum. In lesioned rats, Galphaolf levels were normalized by a 3 week treatment with l-dopa or a D1 agonist but not with aD2-D3 agonist, supporting a Galphaolf regulation by D1 receptor usage. In contrast, the increases of Galphaolf levels in patients were not affected by the duration of l-dopa treatment but correlated with duration of disease. In conclusion, our results revealed in the parkinsonian putamen a prolonged elevation of Galphaolf levels that may lead to a persistent D1 receptor hypersensitivity and contribute to the genesis of long-term complications of L-dopa.
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