Cover legend: The cover illustration shows an artistically modified two-photon fluorescence image of a dendrite and a synaptic spine of a cortical layer 2/3 pyramidal neuron. The Ca²⁺ dependence of the synaptic modifications for spike-timing-dependent plasticity induction protocols was investigated in spines on basal dendrites. It was found that the peak Ca²⁺ transient amplitude alone is not sufficient to account for the direction of the change in synaptic efficacy. It determines the magnitude, but the direction of the change is controlled via a metabotropic glutamate receptor-coupled signaling cascade, which acts in conjunction with voltage-dependent calcium channels and phospholipase C as a sequence coincidence detector that detects post-before-presynaptic action potentials resulting in long-term depression. Long term potentiation is induced by activation of NMDA receptors. Thus, presumably two different coincidence detectors in spines control the induction of spike-timing-dependent synaptic plasticity. For more information, see the article by Nevian and Sakmann in the October 25, 2006 issue (pages 11001–11013).