ArticleCNS neuroscience & therapeutics2025
Electrophysiological Alterations in the Progression of Parkinson's Disease and the Therapeutic Effect of Tetrabenazine on Rats With Levodopa-Induced Dyskinesia.
Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Levodopa and Plant-Derived Bioactive Compounds in Parkinson's Disease: Mechanisms, Efficacy, and Future Perspectives.CNS neuroscience & therapeutics · 2025Pooled it
- Aberrant Gamma Oscillations in Parkinson's Disease.Neuroscience bulletin · 2026Review
- The Distinct Electrophysiological Mechanisms in the Cortico-Striatal Circuit of LID Rats.Biology · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
aimsDopamine replacement therapy is the backbone of Parkinson's disease (PD) treatment. However, long-term levodopa (L-DOPA) administration can lead to the severely disabling motor complication L-DOPA-induced dyskinesia (LID), for which standard, effective therapy is currently lacking. This study was conducted to characterize the distinct neural electrophysiological patterns involved in the progression of PD and to examine the efficacy of tetrabenazine, a vesicular monoamine transporter-2 inhibitor, in alleviating dyskinesia and its underlying electrophysiological mechanism.
methodsElectrophysiological analysis was performed to obtain power spectrum density and functional connectivity information from local field potential (LFP) data recorded from the primary motor cortex (M1) and dorsolateral striatum (DLS) during different pathological states in PD model rats. Behavioral tests and abnormal involuntary movements (AIMs) scoring were conducted to confirm PD model establishment and assess LID severity.
resultsIncreased beta oscillations and abnormally strengthened beta causality in the M1 → DLS direction and exaggerated beta-band M1-DLS functional connectivity were observed in the PD state. L-DOPA administration suppressed beta activity and augmented gamma power in the M1 and DLS, with increased gamma causality in the M1 → DLS direction and beta causality in the DLS → M1 direction, as well as elevated gamma-band M1-DLS functional connectivity. Tetrabenazine strongly ameliorated dyskinetic manifestations. It suppressed gamma power in the M1 and DLS, reduced gamma causality and increased beta causality in the M1 → DLS direction, reduced beta causality in the DLS → M1 direction, and reduced gamma-band M1-DLS functional connectivity.
conclusionTetrabenazine abrogated aberrant gamma activity to improve LID symptoms, which provides compelling evidence for its future clinical application in LID therapy.
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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.