Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model.

@article{Wangemann2007LossOC,
  title={Loss of cochlear HCO3- secretion causes deafness via endolymphatic acidification and inhibition of Ca2+ reabsorption in a Pendred syndrome mouse model.},
  author={Philine Wangemann and Kazuyasu Nakaya and Tao Wu and Rajanikanth J Maganti and Erin M Itza and Joel D. Sanneman and Donald G. Harbidge and Sara E. Billings and Daniel C Marcus},
  journal={American journal of physiology. Renal physiology},
  year={2007},
  volume={292 5},
  pages={
          F1345-53
        }
}
Pendred syndrome, characterized by childhood deafness and postpuberty goiter, is caused by mutations of SLC26A4, which codes for the anion exchanger pendrin. The goal of the present study was to determine how loss of pendrin leads to hair cell degeneration and deafness. We evaluated pendrin function by ratiometric microfluorometry, hearing by auditory brain stem recordings, and expression of K(+) and Ca(2+) channels by confocal immunohistochemistry. Cochlear pH and Ca(2+) concentrations and… CONTINUE READING

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