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| Paper IPM / Biological / 17297 |
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Parkinsonâs disease (PD) is associated with abnormal beta band oscillations (13â30 Hz) in the corticobasal 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 defcits 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, 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 is able to quench the pathological
synchrony and beta oscillations, while, applying inhibitory DBS failed to quench the PD signs. In light of
simulation results, we conclude that the effect of the DBS on its target is excitatory.
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