Abstract
Auditory sensory outer hair cells are thought to amplify sound-induced basilar membrane vibration through a feedback mechanism to enhance hearing sensitivity. For optimal amplification, the outer hair cell-generated force must act on the basilar membrane at an appropriate time at every cycle. However, the temporal relationship between the outer hair cell-driven reticular lamina vibration and the basilar membrane vibration remains unclear. By measuring sub-nanometer vibrations directly from outer hair cells using a custom-built heterodyne low-coherence interferometer, we demonstrate in living gerbil cochleae that the reticular lamina vibration occurs after, not before, the basilar membrane vibration. Both tone- and click-induced responses indicate that the reticular lamina and basilar membrane vibrate in opposite directions at the cochlear base and they oscillate in phase near the best-frequency location. Our results suggest that outer hair cells enhance hearing sensitivity through a global hydromechanical mechanism, rather than through a local mechanical feedback as commonly supposed.
Highlights
This paper reports the first in vivo measurement of the latency difference between the outer hair cell-driven reticular lamina vibration and the basilar membrane vibration
The present data demonstrate that the latency of the reticular lamina vibration is greater than that of the basilar membrane vibration, and there is no significant phase difference between the two structures near the best frequencies
This result is consistent with the mouse data measured using heterodyne interferometry (Ren et al, 2016b) but inconsistent with the guinea pig data, which showed that the phase of the reticular lamina vibration leads the phase of the basilar membrane vibration by ~90 ̊ at the best frequency and the phase lead decreases with sound pressure level (Chen et al, 2011)
Summary
The exceptional sensitivity of mammalian hearing has been attributed to a micromechanical feedback system inside the cochlea, called ‘the cochlear amplifier’ or ‘cochlear active process’ (Dallos et al, 2008; Davis, 1983; Fettiplace and Hackney, 2006; Hudspeth, 2014; Robles and Ruggero, 2001; Russell et al, 2007). In response to the membrane potential change, mammalian outer hair cells change their length and generate force primarily through the somatic motility driven by the motor protein, prestin (Ashmore, 2008; Brownell et al, 1985; Liberman et al, 2002; Mammano and Ashmore, 1993; Mellado Lagarde et al, 2008; Ren et al, 2016a; Santos-Sacchi, 1989; Zheng et al, 2000) This cellular force is thought to be directly applied to the basilar membrane at its generation location on a cycle-by-cycle basis, amplifying the sound-induced basilar membrane vibration and boosting hearing sensitivity (Dallos et al, 2008; de Boer, 1995b; Dong and Olson, 2013; Hudspeth, 2014; Liu and Neely, 2009; Reichenbach and Hudspeth, 2014).
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