ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Deafness and permanently reduced potassium channel gene expression and function in hypothyroid Pit1dw mutants.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 2 of them syntheses that pooled it.
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Who cites it
42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 74 citations in OpenAlex.
- A Systematic Review of Genes Affecting Endocochlear Potential.Journal of the Association for Research in Otolaryngology : JARO · 2026Pooled it
- A Systematic Review on the Role of the Stria Vascularis in Menière's Disease Pathogenesis.Journal of the Association for Research in Otolaryngology : JARO · 2025Pooled it
- The Role of Thyroid Hormone Signaling in the Development and Pathophysiology of Hearing: From Molecular Mechanisms to Clinical Applications.International journal of molecular sciences · 2026Review
- Tectorial membrane: structure, function, and its implications for hearing loss.Frontiers in neurology · 2025Review
- Common and Uncommon Mouse Models of Growth Hormone Deficiency.Endocrine reviews · 2024Review
- The Dual Roles of Triiodothyronine in Regulating the Morphology of Hair Cells and Supporting Cells during Critical Periods of Mouse Cochlear Development.International journal of molecular sciences · 2023Article
- The Roles of Solute Carriers in Auditory Function.Frontiers in genetics · 2022Review
- Kölliker's organ-supporting cells and cochlear auditory development.Frontiers in molecular neuroscience · 2022Review
- Cochlear Fibrocyte and Osteoblast Lineages Expressing Type 2 Deiodinase Identified with a Dio2CreERt2 Allele.Endocrinology · 2021Article
- Review
- Thyroid Hormone Deiodinases: Dynamic Switches in Developmental Transitions.Endocrinology · 2021Review
- Mouse models of growth hormone deficiency.Reviews in endocrine & metabolic disorders · 2021Review
- Exacerbated age-related hearing loss in mice lacking the p43 mitochondrial T3 receptor.BMC biology · 2021Article
- Programmed Cell Death Recruits Macrophages Into the Developing Mouse Cochlea.Frontiers in cell and developmental biology · 2021Article
- An Age-Related Hearing Protection Locus on Chromosome 16 of BXD Strain Mice.Neural plasticity · 2020Article
- TSP1 and TSP2 Have Unique and Overlapping Roles in Protecting against Noise-Induced Auditory Synaptopathy.Neuroscience · 2019Article
- Genetic variation in thyroid folliculogenesis influences susceptibility to hypothyroidism-induced hearing impairment.Mammalian genome : official journal of the International Mammalian Genome Society · 2019Article
- Deafness and loss of cochlear hair cells in the absence of thyroid hormone transporters Slc16a2 (Mct8) and Slc16a10 (Mct10).Scientific reports · 2018Article
- Article
- GC-B Deficient Mice With Axon Bifurcation Loss Exhibit Compromised Auditory Processing.Frontiers in neural circuits · 2018Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
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 beta-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.
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