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input. The dynamics of and bifurcations in the models were studied by computational and analytical techniques. There is an experimental evidence for how dopamine presynaptically suppresses different types of basal ganglia synapses. We show how the chance in strength of dopamine-modulated synapses promotes intermittent synchronous activity patterns under very general conditions and investigate the cellular properties, necessary for this dynamics. It is also known that dopamine affects not only synaptic properties, but also cellular properties of BG neurons. In particular, change in the dopaminergic status leads to change in the temporal features of firing patterns of STN neuron. So we also considered how dopaminedependent features of STN neuron firing modulate the GPe response and the synchrony between STN input and GPe output. As STN dopaminergic modulation and STN activity pattern vary, we observe the overall transition from low coherence state to high coherence state through intermittent synchronous activity. This points to the important role of GPe cells within BG circuit and demonstrate that the response of GPe cell, which was achieved through the interaction between the intrinsic properties of the cell itself and membrane properties of STN cell, provide good source for the temporal characteristics of synchrony observed in experimental setting. In sum, our modeling studies explain how the lack of dopamine in Parkinson’s disease may lead to the generation of intermittent synchronous dynamics in the basal ganglia via two different pathways: cellular and synaptic.

Mechanisms of pathological synchrony in Parkinson's disease induced by changes in synaptic and cellular properties due to dopamine