Noise priming and the effects of different cochlear centrifugal pathways on loud-sound-induced hearing loss.
Priming/conditioning the cochlea with moderately loud sound can reduce damage caused by subsequent loud sound. This study examined immediate effects of short-term priming with monaural broadband noise on temporary threshold shifts (TTSs) in hearing caused by a subsequent loud high-frequency tone and the role of centrifugal olivocochlear pathways. Priming caused delay-dependent changes in tone-induced TTSs, particularly or only at frequencies higher than the peak tone-affected frequency, through two general effects: a short-lasting increase in cochlear susceptibility to loud sound and longer-lasting complex end effects of centrifugal pathways. The results indicated the following points. Priming noise had "pure" cochlear effects, outlasting its presentation and declining with delay, that exacerbated tone-induced TTSs at frequencies higher than the peak tone-affected frequency. The centrifugal uncrossed medial olivocochlear system (UMOCS) could prevent this noise exacerbation and as this noise effect declined, could even reduce tone-induced TTSs below those to the unprimed tone. For longer delays, when priming noise no longer had any exacerbative "pure" cochlear effects on TTSs, UMOCS exacerbated TTSs above those to the unprimed tone. The crossed medial olivocochlear system (CMOCS) appeared to show a gradual "build-up" of effects postpriming. A parallel study showed it exercised no end effect on TTSs when noise and tone were concurrent. With priming, CMOCS effects were observed. For the shortest priming delay, the CMOCS blocked a UMOCS effect preventing noise exacerbation of tone-induced TTSs. For longer delays, CMOCS end effects, when present, reduced tone-induced TTSs below those to the unprimed tone. The CMOCS may oscillate between producing these effects and exerting no end-effect. With increasing delay CMOCS protection occurred in a greater proportion of animals. Finally, with a delay of 600 s between primer and loud tone, all these systems appeared to have reset to normal so that TTSs were similar to those in the unprimed condition. Thus the effects of short-term priming are not simple and do not suggest that centrifugal pathways act automatically as a protective system during such priming.
Rajan
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Department of Physiology, Monash University, Monash, VIC 3800, Australia. ramesh.rajan@med.monash.edu.au
D000222:Adaptation, Physiological / Q000502:physiology; D000818:Animals; D001306:Auditory Pathways / Q000166:cytology / Q000502:physiology*; D001309:Auditory Threshold / Q000502:physiology; D002415:Cats; D003051:Cochlea / Q000166:cytology / Q000293:injuries / Q000503:physiopathology*; D003213:Conditioning, Psychological / Q000502:physiology*; D006317:Hearing Loss, Noise-Induced / Q000503:physiopathology* / Q000517:prevention & control; D009622:Noise; D009847:Olivary Nucleus / Q000166:cytology / Q000502:physiology