Synapses exhibit many forms of plasticity that occur over a broad temporal range. At the shortest times (milliseconds to minutes), facilitation, augmentation, potentiation, and depression provide rapid but transient modifications in synaptic transmission. These forms of plasticity change the amount of neurotransmitter released from presynaptic terminals and are based on alterations in Ca²⁺ signaling and synaptic vesicle pools at recently active terminals. Longer-lasting forms of synaptic plasticity such as LTP and LTD are also based on Ca²⁺ and other intracellular second messengers. At least some of the synaptic changes produced by these long-lasting forms of plasticity are postsynaptic, caused by changes in neurotransmitter receptor trafficking, although alterations in neurotransmitter release from the presynaptic terminal can also occur. In these more enduring forms of plasticity, protein phosphorylation and changes in gene expression greatly outlast the period of synaptic activity and can yield changes in synaptic strength that persist for hours, days, or even longer. Long-lasting synaptic plasticity can serve as a neural mechanism for many forms of brain plasticity, such as learning new behaviors or acquiring new memories.