4.4 Article

Sensory transduction and adaptation in inner and outer hair cells of the mouse auditory system

Journal

JOURNAL OF NEUROPHYSIOLOGY
Volume 98, Issue 6, Pages 3360-3369

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00914.2007

Keywords

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Funding

  1. NIDCD NIH HHS [R01 DC005439-05, DC05439, R01 DC005439, R56 DC005439] Funding Source: Medline

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Sensory transduction and adaptation in inner and outer hair cells of the mouse auditory system. J Neurophysiol 98: 3360-3369, 2007. First published October 17, 2007; doi:10.1152/jn.00914.2007. Auditory function in the mammalian inner ear is optimized by collaboration of two classes of sensory cells known as inner and outer hair cells. Outer hair cells amplify and tune sound stimuli that are transduced and transmitted by inner hair cells. Although they subserve distinct functions, they share a number of common properties. Here we compare the properties of mechanotransduction and adaptation recorded from inner and outer hair cells of the postnatal mouse cochlea. Rapid outer hair bundle deflections of about 0.5 micron evoked average maximal transduction currents of about 325 pA, whereas inner hair bundle deflections of about 0.9 micron were required to evoke average maximal currents of about 310 pA. The similar amplitude was surprising given the difference in the number of stereocilia, 81 for outer hair cells and 48 for inner hair cells, but may be reconciled by the difference in single-channel conductance. Step deflections of inner and outer hair bundles evoked adaptation that had two components: a fast component that consisted of about 60% of the response occurred over the first few milliseconds and a slow component that consisted of about 40% of the response followed over the subsequent 20-50 ms. The rate of the slow component in both inner and outer hair cells was similar to the rate of slow adaptation in vestibular hair cells. The rate of the fast component was similar to that of auditory hair cells in other organisms and several properties were consistent with a model that proposes calcium-dependent release of tension allows transduction channel closure.

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