Prestin-based outer hair cell motility is necessary for mammalian cochlear amplification.
It is a central tenet of cochlear neurobiology that mammalian ears rely on a local, mechanical amplification process for their high sensitivity and sharp frequency selectivity. While it is generally agreed that outer hair cells provide the amplification, two mechanisms have been proposed: stereociliary motility and somatic motility. The latter is driven by the motor protein prestin. Electrophysiological phenotyping of a prestin knockout mouse intimated that somatic motility is the amplifier. However, outer hair cells of knockout mice have significantly altered mechanical properties, making this mouse model unsatisfactory. Here, we study a mouse model without alteration to outer hair cell and organ of Corti mechanics or to mechanoelectric transduction, but with diminished prestin function. These animals have knockout-like behavior, demonstrating that prestin-based electromotility is required for cochlear amplification.
Pubmed ID: 18466744 RIS Download
Action Potentials | Animals | Auditory Threshold | Cell Movement | Cilia | Hair Cells, Auditory, Outer | Hearing | Mammals | Mechanotransduction, Cellular | Mice | Mice, Knockout | Mice, Mutant Strains | Models, Animal | Molecular Motor Proteins