Abstract

The mechanism of mammalian hearing has intrigued scientists for decades. It is widely assumed that the process of hearing begins when sound reaches the inner ear and causes the basilar membrane (BM) to vibrate. These vibrations are then detected and consequently amplified by the outer hair cells (OHCs). We question this sequence of events and the inauguration of sound-induced motility, i.e. transformation of sound pressure wave into directional vibrations. Based on the morphology of the mammalian cochlea, we suggest that motility of the OHCs could be due to the synchronized action of hundreds of thousands of nanometric acoustic sensors-actuators in the OHC’s lateral wall. We propose that stochastic resonance in these nanometric units can account for all of the major features of mammalian hearing: a wide dynamic range; sharp frequency selectivity; generation of spontaneous otoacoustic emissions; and the ability to process relatively high frequencies. The proposed model might inspire the design of hypersensitive sensors and actuators, which potentially could be incorporated into new types of hearing aids.

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