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.
KeywordsDopamine Autocorrelation Dura Dopa
Unable to display preview. Download preview PDF.
- Ferrante R.J., Kowall N.W., and Richardson E.P. (1991) Proliferative and degenerative changes in striatal spiny neurons in Huntington’s disease: A combined study using the section-Golgi method and calbindin D28k immunocytochemistry. J. Neurosci., 11:3877–3887Google Scholar
- Harper P.S. (1991) Huntington’s disease. Saunders, LondonGoogle Scholar
- Wilson M.A. and Bower J.M. (1989) The simulation of large-scale neural networks. In: Koch C. and Segev I. (eds.) Methods in Neural Modeling: From Synapses to Networks. MIT Press, Cambridge, 291–334Google Scholar