ArticleNeuron2018
A Subpopulation of Striatal Neurons Mediates Levodopa-Induced Dyskinesia.
Article in Neuron, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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Who cites it
75 citing papers in PubMed, 144 citations in OpenAlex.
- Probing inter-areal computations with a two-photon holographic mesoscope.Nature neuroscience · 2026Article
- Distinct contributions of two subpopulations of subthalamic neurons to levodopa-induced dyskinesia.Science advances · 2026Article
- The GPCR Smoothened on cholinergic interneurons modulates dopamine-associated acetylcholine dynamics, learning, and effort management.iScience · 2026Article
- Microglial sTREM2 limits dyskinesia and acts on TrkB to support circuit plasticity.bioRxiv : the preprint server for biology · 2026Article
- Effects of chemogenetic inhibition of serotonergic raphe-striatal neurons on L-DOPA-induced behaviors and neurochemistry in a rat model of Parkinson's disease.Acta neuropathologica communications · 2026Article
- Cerebrospinal fluid dopamine 3-O-sulfate as a novel biomarker for predicting motor complications in Parkinson's disease: insights from the PPMI cohort.Journal of translational medicine · 2026Article
- Dopamine 2 receptor ablation from cholinergic neurons attenuates L-DOPA induced dyskinesias.Frontiers in aging neuroscience · 2026Article
- Feasibility study of differentiating patients with levodopa-induced dyskinesia using cerebellar gray and white matter radiomics features from 3DT1WI images.Frontiers in aging neuroscience · 2026Article
- Voluntary exercise increases striatal dopamine release and improves motor performance in aging mice.NPJ Parkinson's disease · 2025Article
- State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson's disease.Science advances · 2025Article
- A glutamatergic brain neural circuit is critical for modulating trigeminal neuropathic pain.Pain · 2025Article
- 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
- Cortical Intra-Layer Hypersynchronization in Levodopa-Induced Dyskinesia Mouse Model.Brain and behavior · 2025Article
- A Convergent Pathway for Stimulation-Induced Dyskinesia Following Deep Brain Stimulation.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Erasing "bad memories": reversing aberrant synaptic plasticity as therapy for neurological and psychiatric disorders.Molecular psychiatry · 2025Review
- Repetitive Levodopa Treatment Drives Cell Type-Specific Striatal Adaptations Associated With Progressive Dyskinesia in Parkinsonian Mice.bioRxiv : the preprint server for biology · 2025Article
- Sexual Dimorphism in Levodopa-Induced Dyskinesia Following Parkinson's Disease: Uncharted Territory.The European journal of neuroscience · 2025Review
- State-dependent modulation of spiny projection neurons controls levodopa-induced dyskinesia in a mouse model of Parkinson's disease.bioRxiv : the preprint server for biology · 2025Article
- The basolateral amygdala-anterior cingulate cortex circuit contributes to postherpetic neuralgia-anxiety comorbidity.Theranostics · 2025Article
- Levodopa-induced dyskinesia: brain iron deposition as a new hypothesis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
15 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Parkinson's disease is characterized by the progressive loss of midbrain dopamine neurons. Dopamine replacement therapy with levodopa alleviates parkinsonian motor symptoms but is complicated by the development of involuntary movements, termed levodopa-induced dyskinesia (LID). Aberrant activity in the striatum has been hypothesized to cause LID. Here, to establish a direct link between striatal activity and dyskinesia, we combine optogenetics and a method to manipulate dyskinesia-associated neurons, targeted recombination in active populations (TRAP). We find that TRAPed cells are a stable subset of sensorimotor striatal neurons, predominantly from the direct pathway, and that reactivation of TRAPed striatal neurons causes dyskinesia in the absence of levodopa. Inhibition of TRAPed cells, but not a nonspecific subset of direct pathway neurons, ameliorates LID. These results establish that a distinct subset of striatal neurons is causally involved in LID and indicate that successful therapeutic strategies for treating LID may require targeting functionally selective neuronal subtypes.
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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.