Abstract
Exaggerated beta oscillations (~13-30 Hz) observed in the cortical areas of the brain is one of the characteristics of disrupted information flow in the primary motor cortex in Parkinson's disease (PD). However, the mechanism underlying the generation of these enhanced beta rhythms remains unclear. The thalamo-cortex microcircuit (TCM) contains reciprocal synaptic connections that generate low frequency oscillations in the microcircuit in healthy conditions. Recent studies suggest that alterations in synaptic connections both within and between the cortex and thalamus play a critical role in the generation of pathological beta rhythms in PD. In this study, we examine this hypothesis in a spiking neuronal network model of the TCM. The model is compared and validated against neural firing patterns recorded in rodent models of PD from the literature.
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