Ribbon synapses of inner hair cells (IHCs) undergo developmental maturation until after the onset of hearing. Here, we studied whether IHC synaptogenesis is regulated by thyroid hormone (TH). We performed perforated patch-clamp recordings of Ca2+ currents and exocytic membrane capacitance changes in IHCs of athyroid and TH-substituted Pax8-/- mice during postnatal development. Ca2+ currents remained elevated in athyroid IHCs at the end of the second postnatal week, when Ca2+ influx had developmentally declined in wild-type and TH- rescued mutant IHCs. The efficiency of Ca2+ influx in triggering exocytosis of the readily releasable vesicle pool was reduced in athyroid IHCs. Ribbon synapses were formed despite the TH- deficiency. However, different from wt, where synapse elimination takes place around the onset of hearing, the number of ribbon synapses remained elevated in 2-week-old athyroid IHCs. Moreover, the ultrastructure of these synapses appeared immature. Using quantitative RT-PCR we found a TH-dependent developmental upregulation of the mRNAs for the neuronal SNARE proteins SNAP25 and synaptobrevin 1 in the organ of Corti. These molecular changes probably contribute to the improvement of exocytosis efficiency in mature IHCs. We conclude that TH regulates IHC differentiation and is essential for morphological and functional maturation of their ribbon synapses.