Outer hair cells in the mammalian cochlea and noise-induced hearing loss

Abstract

Hair cells in the mammalian cochlea transduce mechanical stimuli into electrical signals leading to excitation of auditory nerve fibres. Because of their important role in hearing, these cells are a possible site for the loss of cochlear sensitivity that follows acoustic overstimulation. We have recorded from inner and outer hair cells (IHC, OHC) in the guinea pig cochlea during and after exposure to intense tones. Our results show functional changes in the hair cells that may explain the origin of noise-induced hearing loss. Both populations of hair cells show a reduction in amplitude and an increase in the symmetry of their acoustically evoked receptor potentials. In addition, the OHCs also suffer a sustained depolarization of the membrane potential. Significantly, the membrane and receptor potentials of the OHCs recover in parallel with cochlear sensitivity as measured by the IHC receptor potential amplitude and the auditory nerve threshold. Current theories of acoustic transduction suggest that the mechanical input to IHCs may be regulated by the OHCs. Consequently, the modified function of OHCs after acoustic overstimulation may determine the extent of the hearing loss following loud sound.

The structural and functional consequences of acoustic injury in the cochlea and peripheral auditory system: A five year update

“…The first description of hair-cell electrophysiology following exposure to intense sound was reported during the past 5 years (Cody and Russell, 1985, 1988. Receptor potentials from basal turn hair cells in the guinea pig exhibit characteristic responses to sound that have been described elsewhere (Russell and Sellick, 1983;Cody and Russell, 1986;Cody and Russell, 1988).…”

A fast motile response in guinea‐pig outer hair cells: the cellular basis of the cochlear amplifier.

“…Fig. 5A shows that the movements could also be elicited in the physiological membrane potential range between -90 and -70 mV, close to the resting potential of hair cells in vivo (Dallos et al 1982;Cody & Russell, 1985). Fig.…”

Contextual modulation of cochlear hearing desensitization depends on the type of loud sound trauma

“…Studies noted in Section 1 show that TTSs caused by the short-duration moderately intense traumata used here are most likely due to changes in cochlear mechanics caused by a decrease in output of the OHC electromotile ''active'' process (Chertoff et al, 1997;Chan et al, 1998;Cody and Russell, 1985;Cooper and Rhode, 1992;Fridberger et al, 2002a,b;Patuzzi et al, 1984Patuzzi et al, , 1989Patuzzi, 1992Patuzzi, , 1998Ruggero et al, 1993Ruggero et al, , 1996Zhang and Zwislocki, 1995). Then, to account for the WN-induced reduction in TTSs to NB trauma, it can be proposed that the atraumatic WN destructively interferes with BM vibration to the NB traumata.…”

“…The TTSs measured some time (about 5 min) after short-duration moderate-intensity traumata of the recent studies (Rajan, 2000(Rajan, , 2005 are most likely due to changes in cochlear mechanics (Cooper and Rhode, 1992;Fridberger et al, 2002a,b;Patuzzi et al, 1984;Ruggero et al, 1993Ruggero et al, , 1996 caused by a decrease in output of the OHC electromotile ''active'' process (e.g., Patuzzi et al, 1989;Patuzzi, 1992Patuzzi, , 1998Fridberger et al, 2002b;Zhang and Zwislocki, 1995). As nicely summarised by Fridberger et al (2002b), the reduction in OHC amplification that is the basis for such TTSs has been suggested to be due either to effects exerted on forward transduction at the level of the OHC stereocilia or the transduction channels in the stereocilia (e.g., Chertoff et al, 1997;Patuzzi et al, 1989;Patuzzi, 1992Patuzzi, , 1998Ruggero et al, 1993Ruggero et al, , 1996 or changes at the level of the OHC cell bodies (cf., Cody and Russell, 1985;Chan et al, 1998); in either case there is a decrease in the gain of the OHC amplification process. However, nothing in the current literature of cochlear mechanics predicts or explains why the same atraumatic background WN should exacerbate TTSs to a ''point'' stimulus (namely, a pure tone) and reduce it when the trauma was ''dispersed''.…”