4.3 Review

Protection from acoustic trauma is not a primary function of the medial olivocochlear efferent system

Publisher

SPRINGER
DOI: 10.1007/s10162-002-3013-y

Keywords

cochlea; efferent protection; noise-induced hearing loss

Funding

  1. NIDCD NIH HHS [R01 DC001692, DC01692] Funding Source: Medline
  2. NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS [R01DC001692] Funding Source: NIH RePORTER

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The medial olivocochlear (MOC) efferent system is an important component of an active mechanical outer hair cell system in mammals. An extensive neurophysiological literature demonstrates that the MOC system attenuates the response of the cochlea to sound by reducing the gain of the outer hair cell mechanical response to stimulation. Despite a growing understanding of MOC physiology, the biological role of the MOC system in mammalian audition remains uncertain. Some evidence suggests that the MOC system functions in a protective role by acting to reduce receptor damage during intense acoustic exposure. For the MOC system to have evolved as a protective mechanism, however, the inner ears of mammals must be exposed to potentially damaging sources of noise that can elicit MOC-mediated protective effects under natural conditions. In this review we evaluate the possibility that the MOC system evolved to protect the inner car from naturally occurring environmental noise. Our survey of nonanthropogenic noise levels shows that while sustained sources of broadband noise are found in nearly all natural acoustic environments, frequency averaged ambient noise levels in these environments rarely exceed 70 dB SPL. Similarly, sources reporting ambient noise spectra in natural acoustic environments suggest that noise levels within narrow frequency bands are typically low in intensity (<40 dB SPL). Only in rare instances (e.g., during frog choruses) are ambient noise levels sustained at moderately high intensities (similar to70-90 dB SPL). By contrast, all experiments in which an MOC-mediated protective effect was demonstrated used much higher sound intensities to traumatize the cochlea (100-150 dB SPL). This substantial difference between natural ambient noise levels and the experimental conditions necessary to evoke MOC-mediated protection suggests that even the noisiest natural acoustic environments are not sufficiently intense to have selected for the evolution of the MOC system as a protective mechanism. Furthermore, although relatively intense noise environments do exist in nature, they are insufficiently distributed to account for the widespread distribution of the MOC system in mammals. The paucity of high-intensity noise and the near ubiquity of low-level noise in natural environments supports the hypothesis that the MOC system evolved as a mechanism for unmasking biologically significant acoustic stimuli by reducing the response of the cochlea to simultaneous low-level noise. This suggested role enjoys widespread experimental support.

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