Abstract
Background Pathophysiology of Parkinson’s disease (PD) is characterized by increased firing rates of cells in the basal ganglia, a tendency toward bursting and abnormal synchronization in cells of subthalamic nucleus (STN) and globus pallidus pars externa (GPe) [1]. In advanced PD, deep brain stimulation (DBS) can be used to disrupt this pathological activity. The standard protocol for DBS is continuous high frequency stimulation of target cells, such as STN. It has been proposed that short-duration stimulation protocols may also disrupt the pathological activity [2]. The mechanism underlying this protocol is supposedly synaptic plasticity. The goal of this study is to investigate, with a biophysically plausible model, the role of synaptic plasticity in stabilizing firing patterns in the basal ganglia.
Highlights
Pathophysiology of Parkinson’s disease (PD) is characterized by increased firing rates of cells in the basal ganglia, a tendency toward bursting and abnormal synchronization in cells of subthalamic nucleus (STN) and globus pallidus pars externa (GPe) [1]
We use a STN-GPe network model consisting of 8-20 STN and GPe cells connected to each other via a sparse structured architecture [3]
We change the weights of the excitatory projections from STN to GPe with a pre-post spike-timing dependent plasticity (STDP) rule
Summary
Pathophysiology of Parkinson’s disease (PD) is characterized by increased firing rates of cells in the basal ganglia, a tendency toward bursting and abnormal synchronization in cells of subthalamic nucleus (STN) and globus pallidus pars externa (GPe) [1]. Method We use a STN-GPe network model consisting of 8-20 STN and GPe cells connected to each other via a sparse structured architecture [3]. The dynamics of each cell is described by a single-compartment conductance-based model.
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