Thyroid hormone is not necessary for the development of outer hair cell electromotility

Abstract

The outer hair cell (OHC), one of two receptor cell types in the organ of Corti, plays a critical role in mammalian hearing. OHCs enhance basilar membrane motion through a local mechanical feedback process within the cochlea, termed the ‘cochlear amplifier’. It is generally believed that the basis of cochlear amplification is a voltage-dependent electromotile response of OHCs. Measurements of electromotility in developing animals indicate that the onset of motility normally occurs around 7 days after birth in altricial rodents such as gerbils and rats. Thyroid hormone (TH) plays a crucial role in the development of the auditory system. Deficiency of the hormone between the late embryonic stage and the second postnatal week can cause severe hearing loss. Several studies suggest that TH deficiency might also affect the development of the cochlear amplifier. The goal of this study was therefore to examine whether TH was necessary for the development of OHC motility. The organ of Corti of gerbils was dissected out at birth and grown in culture with defined concentration of triiodothyronine (T3), the active ligand for the TH receptor. Motility was measured from OHCs isolated from 7-, 11- and 14-day-old cultures. Motility did indeed develop in OHCs deprived of normal concentration of T3. This suggests that the defective auditory function seen in TH-deficient animals is most likely due to morphological and physiological changes in the cochlea, rather than the motor function of the OHCs.