From parkinsonian thalamic activity to suppression by Deep Brain Stimulation: new insights from computational modeling
نویسندگان
چکیده
This paper presents a computational model of a thalamocortical (TC) relay neuron that is used to explore the behaviour of the basal-ganglia thalamocortical loop in relation to Parkinson’s disease and deep brain stimulation. Low frequency oscillations associated with Parkinson’s disease impair thalamic processing by generating rebound action potentials. In the model the thalamocortical cell receives convergent inhibitory input from basal ganglia containing normal and/or oscillatory characteristics associated with Parkinson’s disease. Without additional inputs rebound activity is generated for even mild parkinsonian input around tremor frequency. Periodic input corresponding to high frequency stimulation was found to suppress this activity for even more prominent parkinsonian input when stimulation amplitude and frequency are chosen within a specific window. While the pathological rebound activity disables the thalamocortical cell to relay excitatory cortical input, a stimulation signal with parameter settings corresponding to this specific window restores the relay functionality of the TC cell. PACS numbers: 87.85.eg,87.85.Tu,87.19.ln
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