The deafness caused by early onset hypothyroidism indicates that thyroid hormone is essential for the development of hearing. We investigated the underlying roles of the TRα1 and TRβ thyroid hormone receptors in the auditory system using receptor-deficient mice. TRα1 and TRβ, which act as hormone-activated transcription factors, are encoded by theThraandThrbgenes, respectively, and both are expressed in the developing cochlea. TRβ is required for hearing because TRβ-deficient (Thrbtm1/tm1) mice have a defective auditory-evoked brainstem response and retarded expression of a potassium current (IK,f) in the cochlear inner hair cells. Here, we show that although TRα1 is individually dispensable, TRα1 and TRβ synergistically control an extended array of functions in postnatal cochlear development. Compared withThrbtm1/tm1mice, the deletion of all TRs inThratm1/tm1Thrbtm1/tm1mice produces exacerbated and novel phenotypes, including delayed differentiation of the sensory epithelium, malformation of the tectorial membrane, impairment of electromechanical transduction in outer hair cells, and a low endocochlear potential. The induction ofIK,fin inner hair cells was not markedly more retarded than inThrbtm1/tm1mice, suggesting that this feature of hair cell maturation is primarily TRβ-dependent. These results indicate that distinct pathways mediated by TRβ alone or by TRβ and TRα1 together facilitate control over an extended range of functions during the maturation of the cochlea.