Modeling Synaptic Plasticity in Hippocampus: A Calcium-Based Approach

Abstract

Multiple stimulation protocols using firing rate and spike-timing correlations have been found to be effective in changing synaptic efficacy by inducing long-term potentiation or depression. In many of those protocols, increases in postsynaptic calcium concentration have been shown to play a crucial role. To which extent the plasticity outcome can be explained by the dynamics of the postsynaptic calcium alone remains unclear. Here, we discuss a minimal calcium-based model of a synapse in which potentiation and depression mechanisms are triggered by calcium. We illustrate that this model gives rise to a large diversity of spike timing-dependent plasticity curves, most of which have been observed experimentally in different systems. It accounts quantitatively for plasticity outcomes evoked by protocols involving patterns with variable spike timing and firing rate in hippocampus and neocortex. Furthermore, we use the model to predict memory decay times and plasticity in the presence of uncorrelated Poisson firing. The calcium model provides a mechanistic understanding of how various stimulation protocols provoke specific synaptic changes through the dynamics of calcium concentration and thresholds implementing in simplified fashion protein signaling cascades, leading to long-term potentiation and long-term depression.