Abstract
The excess of 15-30 Hz (β-band) oscillations in the basal ganglia is one of the key signatures of Parkinson's disease (PD). The STN-GPe network is integral to generation and modulation of β band oscillations in basal ganglia. However, the role of changes in the firing rates and spike bursting of STN and GPe neurons in shaping these oscillations has remained unclear. In order to uncouple their effects, we studied the dynamics of STN-GPe network using numerical simulations. In particular, we used a neuron model, in which firing rates and spike bursting can be independently controlled. Using this model, we found that while STN firing rate is predictive of oscillations, GPe firing rate is not. The effect of spike bursting in STN and GPe neurons was state-dependent. That is, only when the network was operating in a state close to the border of oscillatory and non-oscillatory regimes, spike bursting had a qualitative effect on the β band oscillations. In these network states, an increase in GPe bursting enhanced the oscillations whereas an equivalent proportion of spike bursting in STN suppressed the oscillations. These results provide new insights into the mechanisms underlying the transient β bursts and how duration and power of β band oscillations may be controlled by an interplay of GPe and STN firing rates and spike bursts.
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative brain disease caused by the depletion of dopamine neurons in the substantia nigra pars compacta (SNc) [1]
Animal models have shown that the emergence of β band oscillations is accompanied by a change in the firing rate and spike bursting in both subthalamic nuclei (STN) and globus pallidus externa (GPe) neurons
We investigate the effect of firing rate changes and spike bursting in STN and GPe neurons on the power and duration of β band oscillations
Summary
Parkinson’s disease (PD) is a progressive neurodegenerative brain disease caused by the depletion of dopamine neurons in the substantia nigra pars compacta (SNc) [1]. While the etiology of PD is still debated, the behavioral symptoms of PD are accompanied by various changes in the neuronal activity in Basal Ganglia (BG): e.g, increased firing rate of D2 type dopamine receptors expressing striatal neurons [7,8,9]; increase in spike bursts in striatum, globus pallidus externa (GPe), globus pallidus interna (GPi) and subthalamic nuclei (STN) [8] and increased synchrony in all BG nuclei [10] including striatum [11], GPe [12, 13], STN [14,15,16] and GPi/SNr [12, 17, 18] Besides these changes in neuronal activity, at the population level, there is an increase in the power and duration of β band oscillations (15-30 Hz) in local field potential (LFP) recorded from the basal ganglia of PD patients [14, 18,19,20]. Several experimental results indicate that GPe-STN network plays an integral role in generating and modulating these oscillations [14, 18, 19, 36] and their stimulation have been shown to affect (disrupt/modulate) oscillations [8, 37, 38]
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