AI Article Synopsis

  • Dopamine influences synaptic plasticity in the primary motor cortex (M1) and its effects were studied using a paired associative stimulation (PAS) protocol in patients with Parkinson's disease (PD) and multiple system atrophy (MSA-P).
  • Both patient groups without dopamine therapy showed no significant increase in motor-evoked potentials (MEPs) following the PAS protocol, indicating a lack of cortical plasticity without medication.
  • Dopamine replacement therapy in PD restored the MEP increase, suggesting that it's the activation of the cortico-striatal circuit, rather than dopamine itself, that is crucial for enhancing cortical plasticity in M1.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3643922PMC
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0062515PLOS

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