Cochlear Nerve Myelination in Mice Lacking Thyroid Hormone Transporters

Until the 1970s, the leading cause of preventable intellectual disability was untreated congenital hypothyroidism. Although today every child’s thyroid function is screened at birth and treated if hypothyroid, residual deficits remain, including auditory impairments. However, how thyroid hormone (TH) controls development is poorly understood. Our lab is investigating proteins that mediate the transport of TH across the cell membrane and found mice lacking two TH transporters (Mct8/Oatp1c1) have normal cochlear development, but altered auditory processing. This demonstrated that the speed at which auditory signals pass from the cochlea to the brainstem was delayed. An explanation for these findings is that the auditory pathway is hypomyelinated. Therefore, our experiments are designed to test the hypothesis that auditory deficits observed in animals lacking TH transporters Mct8/Oatp1c1 is due, in part, to altered myelination of the auditory pathway. Nervous and cochlear tissues from wildtype and mutant animals were processed and used to determine the levels of myelination between central and peripheral nervous systems in our experimental groups. Our findings will have three implications. First, it will further define the need for TH and TH transporters in development of auditory function. Second, it will allow for either the prevention of auditory deficits due to lack of TH (hypothyroidism) during development or potentially offer novel modalities for treating low TH-associated deficits. Lastly, these findings may transcend to other disorders, including autism and ADHD, as auditory processing deficits are frequently overlooked or ignored, but are often factors in these well- recognized disorders