Abstract
Appearance of dyskinesia is a common problem of long-term Levodopa (L-DOPA) treatment in Parkinson's disease (PD) patients and represents a major limitation for the pharmacological management of the motor symptoms in the advanced stages of disease. An increasing body of evidence points to dopamine released as a false neurotransmitter from the striatal serotonin terminals as the main pre-synaptic determinant of L-DOPA-induced dyskinesia. Here we review the animal experimental and human clinical data in support of this view, which point to the serotonin system as a promising target for anti-dyskinetic therapy in PD patients under L-DOPA medication.
Original language | English |
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Pages (from-to) | 465-478 |
Number of pages | 14 |
Journal | Progress in Brain Research |
Volume | 172 |
DOIs | |
Publication status | Published - 2008 |
Subject classification (UKÄ)
- Neurosciences
Free keywords
- Animals
- Clinical Trials as Topic
- Dopamine
- Dyskinesia, Drug-Induced
- Humans
- Levodopa
- Parkinson Disease
- Parkinsonian Disorders
- Presynaptic Terminals
- Protein Isoforms
- Receptors, Dopamine
- Receptors, Serotonin
- Serotonin
- Journal Article
- Research Support, Non-U.S. Gov't
- Review