Differences in dopaminergic modulation to motor cortical plasticity between Parkinson's disease and multiple system atrophy.
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Where this comes from
- Record sourced from PubMed, PMID 23658735.
- Also identified by DOI 10.1371/journal.pone.0062515 and PMC identifier 3643922.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Dopamine modulates the synaptic plasticity in the primary motor cortex (M1). To evaluate whether the functioning of the cortico-striatal circuit is necessary for this modulation, we applied a paired associative stimulation (PAS) protocol that comprised an electric stimulus to the right median nerve at the wrist and subsequent transcranial magnetic stimulation of the left M1, to 10 patients with Parkinson's disease (PD) and 10 with multiple system atrophy of the parkinsonian type (MSA-P) with and without dopamine replacement therapy (-on/off). To investigate the M1 function, motor-evoked potentials (MEPs) were measured before and after the PAS. In both patient groups without medication, the PAS protocol failed to increase the averaged amplitude of MEPs. The dopamine replacement therapy in PD, but not in MSA-P effectively restored the PAS-induced MEP increase. This suggests that not the existence of dopamine itself but the activation of cortico-striatal circuit might play an important role for cortical plasticity in the human M1.
Medical subject headings
- Antiparkinson Agents
- Evoked Potentials, Motor
- Levodopa
- Motor Cortex
- Multiple System Atrophy
- Parkinson Disease