The hair cell ribbon synapse is specialized for temporally precise and long-lasting synaptic transmission. I will present current insights into the Ca²⁺ signals regulating exocytosis at this synapse. Presynaptic Ca²⁺ influx occurs at ~ 400 nm sized clusters of ~80 Cav1.3 channels, whose trafficking and function depend on Cavbeta2. Both, Cavalpha1.3 and Cavbeta2 are essential for hearing. The Cav1.3 channels of hair cells show little inactivation due to efficient antagonism of calmodulin-mediated CDI by Ca²⁺ binding proteins. Lack of the cytosolic Ca²⁺ binding proteins parvalbumin-alpha, calbindin and calretinin speeds up CDI and augments sustained exocytosis while leaving fast exocytosis unchanged. Synaptic Ca²⁺ influx causes the build-up of Ca²⁺ domains within few milliseconds that reach low micromolar average concentrations and submicrometer size. The voltage-dependence and amplitude of these Ca²⁺ microdomains display remarkable heterogeneity even within individual IHCs. Analysis of the apparent Ca²⁺ dependence of exocytosis during Ca²⁺ influx indicates that Ca²⁺ nanodomains around one or few channels - that sum-up to the observable microdomains - are the relevant signal triggering exocytosis of synaptic vesicles. This Ca²⁺ influx-secretion coupling supports coding of sounds with high temporal precision already at weak sound intensities.