Noise priming and the effects of different cochlear centrifugal pathways on loud-sound-induced hearing loss

Authors
Citation
R. Rajan, Noise priming and the effects of different cochlear centrifugal pathways on loud-sound-induced hearing loss, J NEUROPHYS, 86(3), 2001, pp. 1277-1288
Citations number
41
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROPHYSIOLOGY
ISSN journal
00223077 → ACNP
Volume
86
Issue
3
Year of publication
2001
Pages
1277 - 1288
Database
ISI
SICI code
0022-3077(200109)86:3<1277:NPATEO>2.0.ZU;2-T
Abstract
Priming/conditioning the cochlea with moderately loud sound can reduce dama ge caused by subsequent loud sound. This study examined immediate effects o f short-term priming with monaural broadband noise on temporary threshold s hifts (TTSs) in hearing caused by a subsequent loud high-frequency tone and the role of centrifugal olivocochlear pathways. Priming caused delay-depen dent changes in tone-induced TTSs, particularly or only at frequencies high er than the peak tone-affected frequency, through two general effects: a sh ort-lasting increase in cochlear susceptibility to loud sound and longer-la sting complex end effects of centrifugal pathways. The results indicated th e following points. Priming noise had "pure" cochlear effects, outlasting i ts presentation and declining with delay, that exacerbated tone-induced TTS s at frequencies higher than the peak tone-affected frequency. The centrifu gal uncrossed medial olivocochlear system (UMOCS) could prevent this noise exacerbation and as this noise effect declined, could even reduce tone-indu ced 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 oliv ocochlear system (CMOCS) appeared to show a gradual "build-up" of effects p ostpriming. 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 preventin g noise exacerbation of tone-induced TTSs. For longer delays, CMOCS end eff ects, when present, reduced tone-induced TTSs below those to the unprimed t one. The CMOCS may oscillate between producing these effects and exerting n o end-effect. With increasing delay CMOCS protection occurred in a greater proportion of animals. Finally, with a delay of 600 s between primer and lo ud tone, all these systems appeared to have reset to normal so that TTSs we re similar to those in the unprimed condition. Thus the effects of short-te rm priming are not simple and do not suggest that centrifugal pathways act automatically as a protective system during such priming.