The hair cell synapse’s precision to code the temporal fine structure of acoustic stimuli is astonishing. For example, our capability to locate sound in space builds on interaural time differences of sound insertion of only hundreds of microseconds. Different from conventional synapses that are driven by action potentials and hence build on strong stimulus-secretion coupling, hair cells code sound of extremely different intensities, but all with a temporal precision that suffices phase locking of the auditory nerve fibres spiking with tonal stimuli up to the low kHz range. In fact, even at sound levels that do not yet elicit a proper onset response of the nerve fibres, fibres preferentially discharge at a fixed time of the sine cycle. Biological mechanisms underlying this high temporal precision of sound coding include: -short membrane time constant and rapid repolarization due to massive potassium conductances, -rapidly gating L-type Ca²⁺ channels, -a large and rapidly replenishing pool of readily releasable synaptic vesicles, -high rates of exocytosis at saturating [Ca²⁺] -a ‘Ca²⁺ nanodomain’ control of release, requiring a close positioning of Ca²⁺ channels and vesicle release sites, which ensure release at high [Ca²⁺], -rapidly-gating glutamate receptors depolarizing small postsynaptic elements to threshold. I will present new findings on hair cell stimulus-secretion coupling, vesicle pool dynamics and their molecular/structural determinants. Combining patch-clamp membrane capacitance measurements, electron microscopy and immunohistochemistry to investigate inner hair cells we obtained estimates for the maximal size of the readily releasable vesicle pool (RRP) and for the number of Ca²⁺ channels at the average ribbon synapse. Operating in the Ca²⁺ nanodomain regime, the hair cell responds to varying stimulus intensities by recruiting different numbers of Ca²⁺ channel-release-site units. This results in a stimulus intensity-defined RRP size. Utilizing mouse genetics we demonstrated that the RRP is strongly diminished in the absence of the synaptic ribbon, which also impairs the synchronous activation of the postsynaptic spiral ganglion neurons. We argue that parallel but statistically independent fusion of several vesicles occurs at the hair cell synapse, reducing the jitter of postsynaptic spike timing.