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Mechanisms of L-DOPA-induced dyskinesia in Parkinson's disease
Published on June 2, 2014 44 min
Other Talks in the Series: Parkinson's Disease
Anatomical organization of the basal ganglia
- Prof. Andre Parent
- Université Laval Quebec City, Quebec, Canada
Promising medical therapies for Parkinson’s disease
- Prof. Robert A. Hauser
- University of South Florida, USA
Deep brain stimulation for Parkinson’s disease
- Prof. Michael S. Okun
- University of Florida, USA
Hello, my name is Angela Cenci. I am a professor of experimental medical research at Lund University in Sweden. This talk is about the mechanisms of levodopa-induced dyskinesia in Parkinson's disease.
Parkinson's disease, as illustrated in slide number two, is a neurodegenerative disorder characterized by some typical motor symptoms such as slow movements, loss of spontaneous movements, muscle rigidity, and resting tremor. These symptoms are due to the degeneration of neurons in the substantia nigra that produce the neurotransmitter dopamine as illustrated in drawing to the left. The dopaminergic neurons project their axons to the large, subcortical nucleus, which is shaded in red in the drawing to the right. This nucleus is called the striatum. And it is the part of the striatum called the putamen that processes motor information from the cortex and requires a normal dopaminergic input for its physiological functions.
Dopamine depletion impairs the processing of motor information in neural pathways that connect the cortex and the basal ganglia. In brief, these neural pathways are indicated in the drawing to the right. The cerebral cortex sends glutamatergic axons to the striatum. The striatum uses the information coming from the cortex to elaborate well-coordinated signals used to select or supress movements and then sends these signals to other parts of the basal ganglia, to the globus pallidus in particular from which messages are then sent out to the rest of the brain.