  Neuronal correlates of Parkinson's disease (PD) include a slowing of the
electroencephalogram (EEG) and enhanced synchrony at 3-7 and 7-30 Hz in the
basal ganglia, thalamus, and cortex. This study describes the dynamics of a
physiologically based mean-field model of the basal ganglia-thalamocortical
system, and shows how it accounts for key electrophysiological correlates of
PD. Its connectivity comprises partially segregated direct and indirect
pathways through the striatum, a hyperdirect pathway involving a
corticosubthalamic projection, thalamostriatal feedback, and local inhibition
in striatum and external pallidum (GPe). In a companion paper, realistic
steady-state firing rates were obtained for the healthy state, and after
dopamine loss modeled by weaker direct and stronger indirect pathways, reduced
intrapallidal inhibition, lower firing thresholds of the GPe and subthalamic
nucleus (STN), a stronger striato-GPe projection, and weaker cortical
interactions. Here we show that oscillations around 5 and 20 Hz can arise with
a strong indirect pathway, which also increases synchrony throughout the basal
ganglia. Further, increased theta power with nigrostriatal degeneration
correlates with reduced alpha power and peak frequency, matching experiments.
Unlike the hyperdirect pathway, the indirect pathway sustains oscillations with
realistic phase relationships. Changes in basal ganglia responses to transient
stimuli accord with experimental data. Reduced cortical gains due to both
nigrostriatal and mesocortical dopamine loss lead to slower cortical activity
changes and may be related to bradykinesia. Finally, increased EEG power found
in some studies may be partly explained by a lower effective GPe firing
threshold, reduced GPe-GPe inhibition, and/or weaker intracortical connections
in PD. Strict separation of the direct and indirect pathways is not necessary
for these results.
