ReviewJournal of neural transmission (Vienna, Austria : 1996)2018
Signal transduction in L-DOPA-induced dyskinesia: from receptor sensitization to abnormal gene expression.
Review in Journal of neural transmission (Vienna, Austria : 1996), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- The Signaling and Pharmacology of the Dopamine D1 Receptor.Frontiers in cellular neuroscience · 2021Pooled it
- Dopamine modulation of aggression.Psychopharmacology · 2026Review
- Preservation of Extracellular and Tissue Dopamine During Tyrosine Hydroxylase Loss in Rat 6-OHDA Parkinson's Model: Selective Compensation Restricted to Substantia Nigra.International journal of molecular sciences · 2026Article
- Article
- Molecular Mechanisms of Dopaminergic Neuron Degeneration in Parkinson's Disease: A Comprehensive Review.Current neuropharmacology · 2026Review
- Bioengineered gut bacterium synthesizing levodopa alleviates motor deficits in models of Parkinson's disease.Cell host & microbe · 2025Article
- Rewarding properties of L-Dopa in experimental parkinsonism are mediated by sensitized dopamine D1 receptors in the dorsal striatum.Molecular psychiatry · 2025Article
- The Interaction of Histamine HPharmaceuticals (Basel, Switzerland) · 2024Review
- Transcranial Magnetic Stimulation Attenuates Dyskinesias and FosB and c-Fos Expression in a Parkinson's Disease Model.Brain sciences · 2024Article
- Reduced striatal M4-cholinergic signaling following dopamine loss contributes to parkinsonian and l-DOPA-induced dyskinetic behaviors.Science advances · 2024Article
- Vilazodone, a Selective Serotonin Reuptake Inhibitor with Diminished Impact on Methylphenidate-Induced Gene Regulation in the Striatum: Role of 5-HT1A Receptor.Molecular neurobiology · 2024Article
- Leucine-rich repeat kinase 2 limits dopamine D1 receptor signaling in striatum and biases against heavy persistent alcohol drinking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024Article
- Translational profiling reveals novel gene expression changes in the direct and indirect pathways in a mouse model of levodopa induced dyskinesia.Frontiers in cellular neuroscience · 2024Article
- Phosphodiesterase 10A (PDE10A): Regulator of Dopamine Agonist-Induced Gene Expression in the Striatum.Cells · 2022Article
- Cerebellar stimulation prevents Levodopa-induced dyskinesia in mice and normalizes activity in a motor network.Nature communications · 2022Article
- Subregion-Specific Regulation of Dopamine D1 Receptor Signaling in the Striatum: Implication for L-DOPA-Induced Dyskinesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Involvement of Autophagy in Levodopa-Induced Dyskinesia.Movement disorders : official journal of the Movement Disorder Society · 2021Article
- Carnosic Acid Alleviates Levodopa-Induced Dyskinesia and Cell Death in 6-Hydroxydopamine-lesioned Rats and in SH-SY5Y Cells.Frontiers in pharmacology · 2021Article
- Circuit Mechanisms of L-DOPA-Induced Dyskinesia (LID).Frontiers in neuroscience · 2021Review
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A large number of signaling abnormalities have been implicated in the emergence and expression of L-DOPA-induced dyskinesia (LID). The primary cause for many of these changes is the development of sensitization at dopamine receptors located on striatal projection neurons (SPN). This initial priming, which is particularly evident at the level of dopamine D1 receptors (D1R), can be viewed as a homeostatic response to dopamine depletion and is further exacerbated by chronic administration of L-DOPA, through a variety of mechanisms affecting various components of the G-protein-coupled receptor machinery. Sensitization of dopamine receptors in combination with pulsatile administration of L-DOPA leads to intermittent and coordinated hyperactivation of signal transduction cascades, ultimately resulting in long-term modifications of gene expression and protein synthesis. A detailed mapping of these pathological changes and of their involvement in LID has been produced during the last decade. According to this emerging picture, activation of sensitized D1R results in the stimulation of cAMP-dependent protein kinase and of the dopamine- and cAMP-regulated phosphoprotein of 32 kDa. This, in turn, activates the extracellular signal-regulated kinases 1 and 2 (ERK), leading to chromatin remodeling and aberrant gene transcription. Dysregulated ERK results also in the stimulation of the mammalian target of rapamycin complex 1, which promotes protein synthesis. Enhanced levels of multiple effector targets, including several transcription factors have been implicated in LID and associated changes in synaptic plasticity and morphology. This article provides an overview of the intracellular modifications occurring in SPN and associated with LID.
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