Excitatory Deep Brain Stimulation Quenches Parkinsonian Signs in the Basal Ganglia and Thalamus

Parkinsons disease (PD) is associated with abnormal {beta} band oscillations (13-30 Hz) in the cortico-basal ganglia circuits. Abnormally increased striato-pallidal inhibition and strengthening the synaptic coupling between subthalamic nucleus (STN) and globus pallidus externa (GPe), due to the loss of dopamine, are considered as the potential sources of {beta} oscillations in the basal ganglia. Deep brain stimulation (DBS) of the basal ganglia subregions is known as a way to reduce the pathological {beta} oscillations and motor deficits related to PD. Despite the success of the DBS, its underlying mechanism is poorly understood and, there is controversy about the inhibitory or excitatory role of the DBS in the literature. Here, we utilized a computational network model of basal ganglia which consists of STN, GPe, globus pallidus interna (GPi), and thalamic neuronal population. This model can reproduce healthy and pathological {beta} oscillations similar to what has been observed in experimental studies. Using this model, we investigated the effect of DBS to understand whether its effect is excitatory or inhibitory. Our results show that the excitatory DBS (EDBS) is able to quench the pathological synchrony and {beta} oscillations, while, applying inhibitory DBS (IDBS) failed to quench the PD signs. In light of simulation results, we conclude that the effect of the DBS on its target is excitatory.