A unicellular mechanism to switch a network behavior from tonic activity to synchronous oscillations

Parkinson’s disease (PD) is a neurodegenerative disorder affecting the basal ganglia (BG), a set of small subcortical nervous system nuclei. The hallmark of the disease is a dopaminergic denervation of the input stage of the BG, altering information patterns along movement-related ganglia-mediated pathways in the brain, inducing therefore movement disorders such as tremor at rest, bradykinesia, akinesia, and rigidity. It is still unclear how dopamine depletion causes those motor symptoms. Experimental studies have shown that abnormally synchronized oscillatory activities- rhythmic bursting activity at the neurocellular level and beta frequency band oscillations at the network level-emerge in PD at multiple levels of the BG-cortical loops and are correlated with motor symptoms. We propose a computational model of the BG using a novel unicellular mechanism to explain the induction of bursting activity and beta band oscillations in the network. We show how a single change in the dopaminergic level at the input stage of the BG can switch the model from its physiological state to the pathological state. This computational model also proposes a simple mechanism for high-frequency deep brain stimulations.