Oscillation dynamics in an extended model of thalamic-basal ganglia

Abstract

The increase in oscillations in beta-band (13–30 Hz) of the basal ganglia (BG) is a hallmark neural dynamic feature of Parkinson’s disease (PD). Physiological studies have shown that striatum microcircuits also play an important role in the pathogenesis of this disease, but the relevant biophysical mechanism still remains unclear. Based on the previous striatal inhibitory model, we propose an extended thalamic-basal ganglia model containing medium spine neurons (MSNs) and fast-spiking interneurons (FSIs). Using this model, we demonstrate here that decreasing M-current conductance of the MSNs results in beta oscillations in the striatum and is transmitted to the globus pallidus pars interna (GPi) neurons through direct and indirect channels. Spectral power of local field potential shows that increased inhibition of GPi and globus pallidus pars externa by striatum also causes oscillatory activity in beta-band of BG, and leads to the bursting oscillations of the GPi neurons. In addition, beta-band oscillations in GPi can emerge because of dopamine depletion. And also, gap junction (GJ) between FSIs regulates the peak activity of GPi neurons through the striatum. Especially, in the Parkinson’s state, removal of GJ can reduce the energy of the beta-band slightly. These results not only highlight the roles of the striatum in controlling but also provide new ideas for studying PD in the future.