A Simplified Model of Long-Term Plasticity in Cerebellar Mossy Fiber-Granule Cell Synapses

We simulated synaptic transmission and modified a simple model of long-term potentiation and long-term depression in order to describe long-term plasticity-related changes in cerebellar mossy fiber-granule cell synapses. In our model, protein autophosphorylation, leading to the maintenance of long-term plasticity, is controlled by Ca2+ entry through the NMDA receptor channels. The observed nonlinearity in the development of long-term changes of EPSP in granule cells is explained by the difference in the rate constants of two independent autocatalytic processes.