We simulated synaptic transmission and modified a simple model of the 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 <$E roman Ca sup 2+> entry through the NMDA receptor channels. The observed nonlinearity in the development of long-term changes of EPSP in granule cells is explained by a difference in the rate constants of two independent autocatalytic processes.

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