Oscillations in the basal ganglia: illustration of a cellular effect at the network level

Parkinson’s disease (PD) is a neuro-degenerative pathology affecting the basal ganglia (BG), a set of small subcortical nervous system nuclei. The hallmark of the disease is a dopaminergic denervation of the striatum, al- tering information patterns along movement-related ganglia-mediated path- ways in the brain. Severe motor symptoms result from the pathological state: tremor at rest, bradykinesia, akinesia, and rigidity. The transition to the disease state correlates with a switch in the firing mode of the neurons in the BG, from tonic pacemaker activity to burst firing. At the network level, macro-electrode recordings reveal excessive oscillations in the beta (8- 30Hz) frequency band. The oscillations generation mechanism and their functional role remain under debate. We propose a network model where a cellular mechanism controls the dynamical state of the network. In our model, the oscillatory state impacts the neural information processing prop- erties of the network. The network model predicts that a single decrease of the dopaminergic level in the parkinsonnian condition switches the network into an abnormal oscillatory dynamical and globally insensitive state. The brief dopaminergic increase prior to voluntary movements suppresses beta oscillations to drive the network to a conductive state to sensory processing and cognition.