Abstract
We simulated synaptic transmission and modified a simple model of long-term potentiation and long-term depression in order to describe the 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.
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Saftenku, E.É. A Simplified Model of Long-Term Plasticity in Cerebellar Mossy Fiber–Granule Cell Synapses. Neurophysiology 34, 216–218 (2002). https://doi.org/10.1023/A:1020723921430
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DOI: https://doi.org/10.1023/A:1020723921430