Abstract
Thyroid hormone receptor β (THRβ) is restricted in expression during early embryogenesis but is highly induced in several tissues, including brain, cochlea, retina, pituitary, liver, and kidney during the postnatal period. This chapter presents a study in which Thrb–/–mice provided a recessive model for the human syndrome of resistance to RTH that exhibited a similar endocrine disorder but which was typically caused by dominant THRβ mutants that were transcriptional inhibitors. Analysis of Thrb–/–mice suggests that antagonism of THRβ-mediated pathways underlies the disorder of the pituitary-thyroid axis. Thrb–/–mice also displayed defective maturation of auditory function, as evidenced by the significantly elevated thresholds required for auditory-evoked brainstem responses. The results indicate that THRβ has certain functions in vivo that cannot be substituted by THRa, implying that the two THR genes serve at least some distinct functions.
Published Version
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