Impacts of a unicellular mechanism on network behaviors

Parkinson’s disease (PD) is a neurodegenerative disorder af- fecting the basal ganglia (BG), a set of small subcortical nervous system nuclei. The hallmark of the disease is a dopaminergic denervation of the striatum—the input stage of the BG—altering information patterns along movement- related ganglia-mediated pathways in the brain. Severe mo- tor symptoms result from the pathological state: tremor at rest, bradykinesia—the slowness and impaired scaling of voluntary movement—and akinesia—the poverty of volun- tary movements. 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 unicellular level and beta frequency band (from 8 to 30Hz) oscillations at the network level—emerge in PD at multiple levels of the BG-cortical loops and correlate with motor symptoms. The mechanisms underlying these pathological beta oscillations remain elu- sive. We propose that a cellular mechanism generates burst- ing activities and beta band oscillations at the network level.