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Related Experiment Videos

Cochlear function in Prestin knockout mice.

M A Cheatham1, K H Huynh, J Gao

  • 1Department of Communication Sciences and Disorders, Northwestern University, 2-240 Frances Searle Building, 2240 Campus Drive, Evanston, IL 60208, USA. m.cheatham@northwestern.edu

The Journal of Physiology
|August 21, 2004
PubMed
Summary
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Mice lacking the Prestin gene show impaired hearing, but their outer hair cells (OHCs) still function. This suggests OHC electromotility is not solely responsible for the cochlear amplifier

Area of Science:

  • Auditory Neuroscience
  • Molecular Biology
  • Physiology

Background:

  • Prestin is a motor protein crucial for outer hair cell (OHC) function.
  • OHC electromotility is believed to be the basis of the cochlear amplifier, enhancing hearing sensitivity and frequency selectivity.
  • Mice lacking Prestin provide a model to investigate the role of OHC electromotility.

Purpose of the Study:

  • To determine if outer hair cell (OHC) electromotility, mediated by Prestin, is essential for cochlear amplifier function.
  • To assess frequency selectivity and the integrity of OHC forward transduction in Prestin-deficient mice.

Main Methods:

  • Gross-potential recordings in mice lacking the Prestin gene.
  • Measurement of compound action potential (CAP) thresholds and input-output functions.

Related Experiment Videos

  • Evaluation of cochlear microphonic, summating potential (SP), and intermodulation distortion.
  • Application of the fluorescent dye AM1-43 to assess hair cell transducer activity.

    • Main Results:

    • Prestin knockout mice exhibited significant shifts in CAP thresholds at 5 kHz and 33 kHz.
    • No frequency selectivity was observed in CAP tuning curves of knockout mice.
    • OHC forward transduction, indicated by SP and intermodulation distortion, was not degraded in knockout mice.
    • AM1-43 uptake confirmed transducer channel activity in both inner and outer hair cells of knockout mice.

    Conclusions:

    • While Prestin is essential for normal hearing sensitivity, its absence does not abolish OHC forward transduction.
    • The data suggest that OHC electromotility, mediated by Prestin, is not the sole determinant of the cochlear amplifier's function.
    • Forward transduction mechanisms in hair cells remain functional even without Prestin-driven electromotility.