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The timescales of the dynamics of a system depend on the combination of the timescales of its components and of its transmission delays. Parkinson’s disease is characterized by the death of dopaminergic neurons and the emergence of strong β -band (15-35Hz) oscillations throughout the basal ganglia nuclei. Here we combine experimental stimulation data from ten studies, that reveal the timing of excitatory and inhibitory events in the basal ganglia circuit, to estimate its set of transmission delays. In doing so, we reveal possible inconsistencies in the existing data, calling for replications, and we propose two possible sets of transmission delays. We then integrate these delays in a model of the primate basal ganglia, that does not rely on direct and indirect pathways’ segregation, and show that, while much attention has been given to the role of the striatal dopaminergic receptors in Parkinson’s disease symptoms, extrastriatal dopaminergic depletion in the external part of the globus pallidus and in the subthalamic nucleus is sufficient to generate β -band oscillations in the high part of the band. More specifically, we show that that D2 and D5 dopamine receptors in these nuclei play opposing roles in the emergence of β -band oscillations, thereby explaining how completely deactivating D5 receptors in the subthalamic nucleus can, paradoxically, cancel oscillations.
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