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J Neurophysiol 93: 1977-1988, 2005; doi:10.1152/jn.00848.2004
0022-3077/05 $8.00
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Contextual Modulation of Olivocochlear Pathway Effects on Loud Sound-Induced Cochlear Hearing Desensitization

R. Rajan

Department of Physiology, Monash University, Monash, Australia

Submitted 18 August 2004; accepted in final form 22 November 2004

This study shows that the cochlear hearing losses [temporary threshold shifts (TTSs)] induced by traumatic sound and the effect of olivocochlear (OC) pathways to the cochlea on these hearing losses depend on the context of the sound. Background atraumatic white noise (WN) has been shown to 1) exacerbate loud-pure-tone-induced TTSs, and 2) promote the modulation of TTSs by the uncrossed OC (UOC) pathways additional to the action on TTSs, elicited by binaural loud tones themselves, by the crossed OC (COC) pathway. Here the same atraumatic WN reduced TTSs caused by loud narrow band sound. It also reduced TTS modulation by OC pathways. The UOC no longer exerted any effects on TTSs, and COC effects were significantly reduced in two discrete frequency bands: low frequencies within the narrow band ("within-band" frequencies) and high frequencies outside the band ("high-side" frequencies). COC effects were unchanged at high frequencies within the band. Despite these reductions in OC effects, because the WN itself reduced TTSs, the total effect of OC pathways and background WN now produced larger TTS reductions, especially at higher frequencies. Thus the modulatory effects of the OC pathways on TTSs depend on how background WN modulates cochlear state. It is postulated that the WN background and the OC pathways both modulate TTSs by acting on the outer hair cells, in a way that promotes the reduction of TTSs caused by the narrow band sound trauma. This joint promotion of a protective end-effect on TTSs to narrow band sound trauma contrasts against the effects seen with pure tone trauma where the same background WN exacerbated TTSs at high-side frequencies.


Address for reprint requests and other correspondence: R. Rajan, Dept. of Physiology, Monash Univ., Monash, Victoria 3800, Australia (E-mail: ramesh.rajan{at}med.monash.edu.au)







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