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• W1971627400 abstract "The absence of thyroid hormone (TH) during late gestation and early infancy can cause irreparable deafness in both humans and rodents. A variety of rodent models have been used in an effort to identify the underlying molecular mechanism. Here, we characterize a mouse model of secondary hypothyroidism, pituitary transcription factor 1 ( Pit1 dw ), which has profound, congenital deafness that is rescued by oral TH replacement. These mutants have tectorial membrane abnormalities, including a prominent Hensen's stripe, elevated β-tectorin composition, and disrupted striated-sheet matrix. They lack distortion product otoacoustic emissions and cochlear microphonic responses, and exhibit reduced endocochlear potentials, suggesting defects in outer hair cell function and potassium recycling. Auditory system and hair cell physiology, histology, and anatomy studies reveal novel defects of hormone deficiency related to deafness: (1) permanently impaired expression of KCNJ10 in the stria vascularis of Pit1 dw mice, which likely contributes to the reduced endocochlear potential, (2) significant outer hair cell loss in the mutants, which may result from cellular stress induced by the lower KCNQ4 expression and current levels in Pit1 dw mutant outer hair cells, and (3) sensory and strial cell deterioration, which may have implications for thyroid hormone dysregulation in age-related hearing impairment. In summary, we suggest that these defects in outer hair cell and strial cell function are important contributors to the hearing impairment in Pit1 dw mice." @default.
• W1971627400 created "2016-06-24" @default.
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• W1971627400 date "2009-01-28" @default.
• W1971627400 modified "2023-09-25" @default.
• W1971627400 title "Deafness and Permanently Reduced Potassium Channel Gene Expression and Function in Hypothyroid<i>Pit1</i>^dwMutants" @default.
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• W1971627400 doi "https://doi.org/10.1523/jneurosci.4957-08.2009" @default.
• W1971627400 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3862029" @default.
• W1971627400 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19176829" @default.
• W1971627400 hasPublicationYear "2009" @default.
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