Voltage and spike timing interact in STDP - a unified model

Clopath Clopath

doi:10.3389/fnsyn.2010.00025

Abstract

A phenomenological model of synaptic plasticity is able to account for a large body of experimental data on spike-timing-dependent plasticity (STDP). The basic ingredient of the model is the correlation of presynaptic spike arrival with postsynaptic voltage. The local membrane voltage is used twice: a first term accounts for the instantaneous voltage and the second one for a low-pass filtered voltage trace. Spike-timing effects emerge as a special case. We hypothesize that the voltage dependence can explain differential effects of STDP in dendrites, since the amplitude and time course of backpropagating action potentials or dendritic spikes influences the plasticity results in the model. The dendritic effects are simulated by variable choices of voltage time course at the site of the synapse, i.e., without an explicit model of the spatial structure of the neuron.

Highlights

For synapses between cortical or hippocampal pyramidal neurons, a presynaptic spike a few milliseconds before a postsynaptic one typically leads to long-term potentiation (LTP) whereas the reverse timing leads to depression (Markram et al, 1997; Bi and Poo, 1998; Sjöström et al, 2001), but other preparations exhibit a wide range of other dependencies upon spike timing (Bell et al, 1997; Debanne et al, 1998; Abbott and Nelson, 2000)
The combination of potentiation and depression leads, in voltage clamp experiments, to a voltage dependence shown in Figure 1C which is reminiscent of that found in earlier studies on voltage dependence of synaptic plasticity (Kelso et al, 1986; Artola et al, 1990; Ngezahayo et al, 2000)
In a simulated Spike-timing-dependent plasticity (STDP) experiment, a single post-pre spike pairing leads to LTD if the time difference is short enough, but no plasticity is induced if the timing difference is too big or if the time is inversed (Figures 1A,B)

Summary

Introduction

Spike-timing-dependent plasticity (STDP; Bell et al, 1997; Markram et al, 1997; Bi and Poo, 1998; Sjöström et al, 2001) is induced for most synapses by stimulating pairs of pre- and postsynaptic spikes. Plasticity can be induced in the absence of postsynaptic firing, e.g., in voltageclamp experiments (Kelso et al, 1986; Artola et al, 1990; Ngezahayo et al, 2000) None of these aspects is taken into account in classical phenomenological STDP models (Gerstner et al, 1996; Kempter et al, 1999; Roberts, 1999; Song et al, 2000). Modifications of the classical STDP models including weight-dependence (Kistler and van Hemmen, 2000; van Rossum et al, 2000; Rubin et al, 2001) or alternative summation schemes (Izhikevich, 2003), introduction of frequency dependence (Froemke and Dan, 2002) or some voltage dependence (Brader et al, 2007) resolve at most one or two of the above issues, but not all of them

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Conclusion