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Rating L-DOPA-Induced Dyskinesias in the Unilaterally 6-OHDA-Lesioned Rat Model of Parkinson's Disease
Published on: October 4, 2021
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Maladaptive Synaptic Plasticity in L-DOPA-Induced Dyskinesia.
1The National Key Clinic Specialty, Guangdong Provincial Key Laboratory on Brain Function Repair and Regeneration, The Engineering Technology Research Center of Education Ministry of China, Department of Neurosurgery, Zhujiang Hospital, Southern Medical University Guangzhou, China.
Frontiers in Neural Circuits
|January 10, 2017
Summary
L-DOPA-induced dyskinesia (LID) in Parkinson disease (PD) may stem from maladaptive plasticity in brain circuits. Studies show structural changes in medium spiny neurons and motor cortex contribute to LID.
Area of Science:
- Neuroscience
- Neuroplasticity
- Movement Disorders
Background:
- Parkinson disease (PD) treatment with L-DOPA can lead to L-DOPA-induced dyskinesia (LID).
- LID is linked to maladaptive plasticity in corticostriatal synapses and the cortico-basal ganglia (BG) circuitry.
- Structural and functional changes in medium spiny neurons (MSNs) and motor cortex are observed.
Purpose of the Study:
- To review recent studies on maladaptive plastic changes in the cortico-BG loop.
- To explore the role of these changes in the pathophysiology of LID in Parkinson disease.
- To summarize findings in both animal models and human patients.
Main Methods:
- Review of recent scientific literature.
- Analysis of studies investigating morphological and functional plasticity.
- Examination of data from dyskinetic animal models of PD and human PD patients.
Main Results:
- LID is associated with significant morphological plasticity of striatal dendritic spines.
- Cell type-specific structural plasticity of medium spiny neurons (MSNs) is a key feature.
- Aberrant adaptations occur in the primary motor cortex (M1) and basal ganglia (BG) output nuclei.
Conclusions:
- Maladaptive plasticity within the cortico-BG loop is implicated in LID.
- Understanding these plastic changes is crucial for developing better PD treatments.
- Further research on these mechanisms can inform therapeutic strategies for managing dyskinesia.
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