This chapter discusses the presynaptic, Ca2+-dependent mechanisms of short-term enhancement (STE) of synaptic transmission. Synaptic transmission takes place at specialized contact sites, at which the active zone of the presynaptic neuron approaches the postsynaptic density of a postsynaptic neuron. During prolonged action potential (AP) trains, STE of synaptic transmission, like augmentation, and post-tetanic potentiation (PTP) are also observed at many synapses. A framework for understanding in which ways synaptic strength can be modified is the quantal hypothesis of transmitter release, which originated from electrophysiological studies at the neuromuscular junction. Following longer-lasting trains of presynaptic APs, other forms of STE besides facilitation occur. These can be separated from one another by their time course of decay following the trains. Thus, synapses have a wide range of possibilities to fine-tune their signaling properties and short-term plasticity, according to the needs of the neuronal networks in which they operate.