ArticleBritish journal of pharmacology2019
Optostimulation of striatonigral terminals in substantia nigra induces dyskinesia that increases after L-DOPA in a mouse model of Parkinson's disease.
Article in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Levodopa Disrupts Activity Patterns and Encoding of Movement in Striatal Cholinergic Interneurons of Behaving Mice.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Article
- Repetitive Levodopa Treatment Drives Cell Type-Specific Striatal Adaptations Associated With Progressive Dyskinesia in Parkinsonian Mice.bioRxiv : the preprint server for biology · 2025Article
- Bidirectional regulation of levodopa-induced dyskinesia by a specific neural ensemble in globus pallidus external segment.Cell reports. Medicine · 2024Article
- A non-canonical striatopallidal "Go" pathway that supports motor control.Research square · 2023Article
- Involvement of heat shock proteins and parkin/α-synuclein axis in Parkinson's disease.Molecular biology reports · 2022Review
- Continuous dopaminergic stimulation counteracts L-DOPA-induced overactivity of CaExperimental brain research · 2022Article
- Levodopa-induced dyskinesia: a historical review of Parkinson's disease, dopamine, and modern advancements in research and treatment.Journal of neurology · 2022Review
- Current approaches to characterize micro- and macroscale circuit mechanisms of Parkinson's disease in rodent models.Experimental neurology · 2022Review
- Cardiovascular/Stroke Risk Stratification in Parkinson's Disease Patients Using Atherosclerosis Pathway and Artificial Intelligence Paradigm: A Systematic Review.Metabolites · 2022Review
- Striatal DFrontiers in aging neuroscience · 2022Article
- The Role of Protein S-Nitrosylation in Protein Misfolding-Associated Diseases.Life (Basel, Switzerland) · 2021Review
- Abnormal Cortico-Basal Ganglia Neurotransmission in a Mouse Model of l-DOPA-Induced Dyskinesia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Circuit Mechanisms of L-DOPA-Induced Dyskinesia (LID).Frontiers in neuroscience · 2021Review
- Article
- Dopamine D1 receptor signalling in dyskinetic Parkinsonian rats revealed by fiber photometry using FRET-based biosensors.Scientific reports · 2020Article
- 6-Hydroxydopamine lesion and levodopa treatment modify the effect of buspirone in the substantia nigra pars reticulata.British journal of pharmacology · 2020Article
- Research advances on L-DOPA-induced dyskinesia: from animal models to human disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2020Review
- Interneuron NMDA Receptor Ablation Induces Hippocampus-Prefrontal Cortex Functional Hypoconnectivity after Adolescence in a Mouse Model of Schizophrenia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Selective Regulation of 5-HT1B Serotonin Receptor Expression in the Striatum by Dopamine Depletion and Repeated L-DOPA Treatment: Relationship to L-DOPA-Induced Dyskinesias.Molecular neurobiology · 2020Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeL-DOPA-induced dyskinesia (LID) remains a major complication of L-DOPA therapy in Parkinson's disease. LID is believed to result from inhibition of substantia nigra reticulata (SNr) neurons by GABAergic striatal projection neurons that become supersensitive to dopamine receptor stimulation after severe nigrostriatal degeneration. Here, we asked if stimulation of direct medium spiny neuron (dMSN) GABAergic terminals at the SNr can produce a full dyskinetic state similar to that induced by L-DOPA. EXPERIMENTAL APPROACH: Adult C57BL6 mice were lesioned with 6-hydroxydopamine in the medial forebrain bundle. Channel rhodopsin was expressed in striatonigral terminals by ipsilateral striatal injection of adeno-associated viral particles under the CaMKII promoter. Optic fibres were implanted on the ipsilateral SNr. Optical stimulation was performed before and 24 hr after three daily doses of L-DOPA at subthreshold and suprathreshold dyskinetic doses. We also examined the combined effect of light stimulation and an acute L-DOPA challenge. KEY
resultsOptostimulation of striatonigral terminals inhibited SNr neurons and induced all dyskinesia subtypes (optostimulation-induced dyskinesia [OID]) in 6-hydroxydopamine animals, but not in sham-lesioned animals. Additionally, chronic L-DOPA administration sensitised dyskinetic responses to striatonigral terminal optostimulation, as OIDs were more severe 24 hr after L-DOPA administration. Furthermore, L-DOPA combined with light stimulation did not result in higher dyskinesia scores than OID alone, suggesting that optostimulation has a masking effect on LID. CONCLUSION AND IMPLICATIONS: This work suggests that striatonigral inhibition of basal ganglia output (SNr) is a decisive mechanism mediating LID and identifies the SNr as a target for managing LID.
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