Quantifying Cochlear Nerve Myelination in Mice Lacking Thyroid Hormone Transporters

Our lab has been investigating a group of proteins that mediate the transport of thyroid hormone (TH) across the cell membrane and recently found mice lacking two specific TH transporters (Mct8 and Oatp1c1) have normal cochlear development, but altered auditory processing. Specifically, this data demonstrated that the speed at which auditory signals pass from the cochlea to the brainstem were delayed. The experiments performed were 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. After breeding the animals and processing nervous and cochlear tissue, myelin-staining techniques were used to determine the levels of myelination between central and peripheral nervous systems. Our findings will have two important implications. First, this research will further define the need for these transporters in development to produce normal auditory function. Second, it will allow for either the prevention of auditory deficits due to lack of thyroid hormone (hypothyroidism) during development or potentially offer novel modalities for treating deficits associated with low thyroid hormone