  We present an effective model for timing-dependent synaptic plasticity (STDP)
in terms of two interacting traces, corresponding to the fraction of activated
NMDA receptors and the Ca2+ concentration in the dendritic spine of the
postsynaptic neuron. This model intends to bridge the worlds of existing
simplistic phenomenological rules and highly detailed models, constituting thus
a practical tool for the study of the interplay between neural activity and
synaptic plasticity in extended spiking neural networks. For isolated pairs of
pre- and postsynaptic spikes the standard pairwise STDP rule is reproduced,
with appropriate parameters determining the respective weights and time scales
for the causal and the anti-causal contributions. The model contains otherwise
only three free parameters which can be adjusted to reproduce triplet
nonlinearities in both hippocampal culture and cortical slices. We also
investigate the transition from time-dependent to rate-dependent plasticity
occurring for both correlated and uncorrelated spike patterns.
