Correlated inputs to striatal population drive subthalamic nucleus hyper-synchronization

Abstract

Movement disorders such as Parkinson's disease (PD) are often associated with hyper-synchronization in basal ganglia (BG) activity. The origins of the hyper-synchronization and its interaction with deep brain stimulations (DBS) of BG nuclei are still debated. The structure of the BG suggests that strong neuronal correlations cannot arise within the BG but should rather be inherited from cortical or thalamic inputs. However, this is inconsistent with the hypothesized decorrelating role of the striatal network. Here we investigate to what extent striatum can decorrelate correlated inputs, and the consequences of correlations in striatal activity on the dynamics of the BG; especially, the beta-band oscillations, which are the cardinal symptom of PD. We developed a BG network model with spiking neurons and analyzed the effects on input correlation on BG activity. We found that striatum does not completely decorrelate the inputs and that the residual correlations can synchronize the whole BG. These results provide new insights into the origin of BG hyper-synchronization and pave the way to understand DBS induced disruption of synchrony and ensuing therapeutical effects.