Recently there have been exciting advances in understanding the mechanisms and functional roles of a form of short-term synaptic enhancement (STE) that results from an activity-dependent accumulation of Ca2+ in the presynaptic terminal. This form of STE is composed of at least four processes: fast-decaying facilitation (FI), slow-decaying facilitation (F2), augmentation (AUG) and post-tetanic potentiation (PTP). Recent results suggest that these processes can now be distinguished mechanistically by the site of their induction within the presynaptic terminal: FI and F2 appear to be induced by a rapid, high concentration of Ca2+ at or near the site of exocytosis, whereas AUG and PTP seem to be induced by lower levels of Ca2+ with slower kinetics, possibly within the core of the terminal. STE is highly conserved across diverse species, and appears to serve as a flexible mechanism for temporal information processing in systems ranging from peripheral motor control to higher cortical integration.