ArticleNeuropharmacology2025
Striatal GluN2A gene suppression reduces L-DOPA-induced abnormal involuntary movements in parkinsonian rats.
Article in Neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Electroconvulsive Therapy Induces Dopaminergic Axon Regeneration, Corticostriatal Remodeling, and Restoration of Motor Function in Parkinsonian Mice.bioRxiv : the preprint server for biology · 2025Article
- Involvement of Neuroinflammation and Oxidative Stress in L-DOPA-Induced Dyskinesia in Parkinson's Disease: Role of Renin-Angiotensin System and ROCK Pathway.Antioxidants (Basel, Switzerland) · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
L-DOPA-induced dyskinesia (LID) is a common disabling complication of long-term L-DOPA therapy in Parkinson's disease (PD). LID development is associated with maladaptive plasticity mechanisms in striatal circuits contributed by dysregulated dopamine and glutamate signaling. Upregulation of the NMDAR subunit 2A (GluN2A) over chronic L-DOPA treatment is thought to play a role in corticostriatal synaptic changes. We investigated the motor effects of selective GluN2A gene silencing by injecting a shRNA vector in the striatum of hemiparkinsonian rats. Striatal GluN2A knockdown significantly reduced abnormal involuntary movements (AIMs) while sustaining the therapeutic benefit of L-DOPA. These findings suggest that targeted adjustments of striatal NMDAR subunit composition may be a promising strategy for managing the long-term therapy of PD.
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