Repetitive nerve activity induces various forms of short-term synaptic plasticity that have important computational roles in neuronal networks. Several forms of short-term plasticity are caused largely by changes in transmitter release, but the mechanisms that underlie these changes in the release process have been difficult to address. Recent studies of a giant synapse - the calyx of Held - have shed new light on this issue. Recordings of Ca2+ currents or Ca2+ concentrations at nerve terminals reveal that regulation of presynaptic Ca2+ channels has a significant role in three important forms of short-term plasticity: short-term depression, facilitation and post-tetanic potentiation.
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