A Model of Spike-Timing-Dependent Plasticity

Abstract

It has been shown that postsynaptic calcium dynamics plays an important role in spike timing-dependent plasticity (STDP), a process in which changes in synaptic strength are determined by the relative timing of pre- and postsynaptic activity. It has been suggested STDP involves a postsynaptic chemical network with stable states corresponding to long term potentiation (LTP) and long term depression (LTD). It is believed that the switching of this network between these states is driven by the postsynaptic Ca2+ concentration, but the manner in which the Ca2+ dynamics causes the switching to depend on the relative timing of pre- and postsynaptic activity remains unclear. We describe a model of STDP that combines the chemical network model of Pi and Lisman (2008), with a model of Ca2+ dynamics that builds on the work of Shouval and coworkers (2002). Following Shouval and coworkers, we assume that a portion of the influx of postsynaptic Ca2+ is controlled by NMDA receptors that allow an inward Ca2+ current in response to both glutamate binding and a back propagating action potential (BPAP). To this we add a contribution from voltage dependent calcium channels (VDCCs). We show that this model is able to reproduce the observed time dependence of STDP when a single presynaptic pulse is either followed or preceded by a single BPAP. The behavior of the model with triplet pulse protocols, e.g., two presynaptic pulses separated by a BPAP, or two BPAPs separated by a presynaptic pulse, and the incorporation of more sophisticated models of AMPA trafficking are also described.Pi, H. J. and Lisman, J. E. (2008) J. Neurosci 28: 13132-13138.Shouval, H. Z., Bear, M. F., and Cooper, L. N. (2002) Proc. Natl. Acad. Sci. USA 99: 10831-10836.