  Neural activity in the brain of parkinsonian patients is characterized by the
intermittently synchronized oscillatory dynamics. This imperfect
synchronization, observed in the beta frequency band, is believed to be related
to the hypokinetic motor symptoms of the disorder. Our study explores potential
mechanisms behind this intermittent synchrony. We study the response of a
bursting pallidal neuron to different patterns of synaptic input from
subthalamic nucleus (STN) neuron. We show how external globus pallidus (GPe)
neuron is sensitive to the phase of the input from the STN cell and can exhibit
intermittent phase-locking with the input in the beta band. The temporal
properties of this intermittent phase-locking show similarities to the
intermittent synchronization observed in experiments. We also study the
synchronization of GPe cells to synaptic input from the STN cell with
dependence on the dopamine-modulated parameters. Dopamine also affects the
cellular properties of neurons. We show how the changes in firing patterns of
STN neuron due to the lack of dopamine may lead to transition from a lower to a
higher coherent state, roughly matching the synchrony levels observed in basal
ganglia in normal and parkinsonian states. The intermittent nature of the
neural beta band synchrony in Parkinson's disease is achieved in the model due
to the interplay of the timing of STN input to pallidum and pallidal neuronal
dynamics, resulting in sensitivity of pallidal output to the phase of the
arriving STN input. Thus the mechanism considered here (the change in firing
pattern of subthalamic neurons through the dopamine-induced change of membrane
properties) may be one of the potential mechanisms responsible for the
generation of the intermittent synchronization observed in Parkinson's disease.
