It seems that many auditory maturational events are regulated by thyroid hormone since elevation in thyroid hormone level always precedes the onset of hearing in the fetus-neonate; low thyroid activity in the developing human fetus or rat neonate leads to hearing loss; earlier, elevated thyroid levels in rat neonate lead to earlier onset of hearing. The hormone, bound to its receptors in the nucleus, acts as a transcription factor activating genes which lead to the synthesis of several proteins and enzymes involved in the structural and functional development of many tissues (e.g. brain, heart, kidney, skeletal muscle) including the ear. Several types of congenital hearing loss of unexplained etiology may be due to abnormalities in one or more stages of this gene cascade since several types of congenital hearing loss have been shown to involve defects in genes related to these events.

Keywords:
Development, Maturation, Thyroid, Fetus, Neonate, Auditory development, Cochlea
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© 1996 S. Karger AG, Basel
1996
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