Hearing relies on Ca²⁺ influx-triggered exocytosis in cochlear inner hair cells (IHCs). Here we studied the role of the Ca²⁺ channel subunit Ca_Vβ₂ in hearing. Of the Ca_Vβ_1–4 mRNAs, IHCs predominantly contained Ca_Vβ₂. Hearing was severely impaired in mice lacking Ca_Vβ₂ in extracardiac tissues (Ca_Vβ₂^−/−). This involved deficits in cochlear amplification and sound encoding. Otoacoustic emissions were reduced or absent in Ca_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 the Ca_Vβ₂^−/− mice. Still, sizable onset and adapted spike rates were found during suprathreshold stimulation in Ca_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_Vβ₂ has 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.