Effects of Asymmetric Neuronal Connectivity and Dopamine on Striatal Function: Simulation and Analysis of a Model for Huntington’s Disease
The character of burst firing in a simulated network of striatal medium-sized spiny neurons is critically influenced by the symmetry of radial inhibitory interactions and by the size of an after-hyperpolarisation accumulating in a dopamine-dependent manner with prolonged spiking activity. Asymmetric connectivity transforms the normal pattern of stationary burst activity and depending on its type gives rise to a picture of traveling waves and of irregular sequences of activity, respectively. Decreasing the dopamine-dependent after-hyperpolarisation leads to prolonged burst duration, which functionally enhances the network effects of asymmetric connectivity. The implications of this model for explaining the symptom of chorea in Hunting-ton’s disease are discussed.
KeywordsKainic Acid Striatal Neuron Average Firing Rate Inhibitory Conductance Irregular Sequence
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