To elucidate the role of thyroid hormone receptors (TRs) ␣1 and  in the development of hearing, cochlear functions have been investigated in mice lacking TR␣1 or TR. TRs are ligand-dependent transcription factors expressed in the developing organ of Corti, and loss of TR is known to impair hearing in mice and in humans. Here, TR␣1-deficient (TR␣1 ؊/؊ ) mice are shown to display a normal auditory-evoked brainstem response, indicating that only TR, and not TR␣1, is essential for hearing. Because cochlear morphology was normal in TR ؊/؊ mice, we postulated that TR regulates functional rather than morphological development of the cochlea. At the onset of hearing, inner hair cells (IHCs) in wild-type mice express a fast-activating potassium conductance, I K,f , that transforms the immature IHC from a regenerative, spiking pacemaker to a high-frequency signal transmitter. Expression of I K,f was significantly retarded in TR ؊/؊ mice, whereas the development of the endocochlear potential and other cochlear functions, including mechanoelectrical transduction in hair cells, progressed normally.