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, thus constituting a practical tool for the study of the interplay of 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 timescales for the causal and the anticausal contributions. The model contains otherwise only three free parameters, which can be adjusted to reproduce triplet nonlinearities in 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.