Hearing relies on Ca²⁺influx-triggered exocytosis in cochlear inner hair cells (IHCs). Here we studied the role of the Ca²⁺channel subunit Ca_Vβ₂in hearing. Of the Ca_Vβ_1–4mRNAs, IHCs predominantly contained Ca_Vβ₂. Hearing was severely impaired in mice lacking Ca_Vβ₂in extracardiac tissues (Ca_Vβ₂^−/−). This involved deficits in cochlear amplification and sound encoding. Otoacoustic emissions were reduced or absent inCa_Vβ₂^−/−mice, which showed strongly elevated auditory thresholds in single neuron recordings and auditory brainstem response measurements.Ca_Vβ₂^−/−IHCs showed greatly reduced exocytosis (by 68%). This was mostly attributable to a decreased number of membrane-standing Ca_V1.3 channels. Confocal Ca²⁺imaging revealed presynaptic Ca²⁺microdomains albeit with much lower amplitudes, indicating synaptic clustering of fewer Ca_V1.3 channels. The coupling of the remaining Ca²⁺influx to IHC exocytosis appeared unaffected. Extracellular recordings of sound-evoked spiking in the cochlear nucleus and auditory nerve revealed reduced spike rates in theCa_Vβ₂^−/−mice. Still, sizable onset and adapted spike rates were found during suprathreshold stimulation inCa_Vβ₂^−/−mice. This indicated that residual synaptic sound encoding occurred, although the number of presynaptic Ca_V1.3 channels and exocytosis were reduced to one-third. The normal developmental upregulation, clustering, and gating of large-conductance Ca²⁺activated potassium channels in IHCs were impaired in the absence of Ca_Vβ₂. Moreover, we found the developmental efferent innervation to persist in Ca_Vβ₂-deficient IHCs. In summary, Ca_Vβ₂has an essential role in regulating the abundance and properties of Ca_V1.3 channels in IHCs and, thereby, is critical for IHC development and synaptic encoding of sound.