Additivity of loud-sound-induced threshold losses in the cat under conditions of active or inactive cochlear efferent-mediated protection

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Abstract

1. An additivity model for the accretion of cochlear sensorineural hearing losses has been described from studies in the guinea pig cochlea. Among other aspects, the model allows determination of how residual hearing losses after an initial exposure (E1) affect hearing losses to be expected to a subsequent second exposure (E2). In the present study, the model was applied to temporary hearing losses produced in the cat cochlea by loud pure tones at a frequency from 3 to 15 kHz, affecting regions from 2 to 28 kHz. Successive identical exposures, generally with an interexposure interval of ≃35 min, were used to produce compound action potential (CAP) threshold losses. Total losses after E2 were compared with those predicted by the model. Testing was carried out under conditions where olivocochlear bundle (OCB)-mediated protection was or was not activated. (As shown elsewhere, OCB mediated protection is activated by particular binaural exposures, but not monaural exposure, and reduces threshold losses in the binaural condition with intact OCB compared with losses in either the monaural condition, or the binaural condition where the OCB was cut before loud sound.) 2. The additivity model was a very good predictor of total losses under a variety of conditions; different exposure frequencies, monaural and binaural exposures, and with intact or cut OCB pathways. In these exposures, the model's application could be generalized so that as long as residual losses just pre-E2 were well specified in an animal, total losses could be as well predicted using normative data bases of a single exposure with the same parameters. 3. The model also allowed determination of whether OCB-mediated protection was exercised during E2 in dual identical exposures. Expression of protection for E2 depended on whether E1 elicited protection. When tested with monaural (at 7 or 15 kHz) or binaural exposures (at 3 kHz) for which E1 did not elicit protection, neither did E2. However, when tested with a binaural E1 (at 7, 11, or 15 kHz), which activated protection, E2 also elicited protection. In the latter case, for 7- and 11-kHz exposures, the amount of E2 protection increased with total hearing loss, a relationship similar to that seen for single exposures in cat and guinea pig. For 15-kHz exposure, the amount of E2 protection was constant across test frequencies. 4. Finally, a critical observation with 11-kHz exposure was that a binaural E1 eliciting protection was able to 'prime' the OCB so that protection could be elicited by a subsequent monaural E2, which, by itself as a single exposure, does not evoke protection. This result has important implications in terms of the physiology of the protective OCB pathways and clinically in terms of the manner in which loud-sound-induced hearing loss accumulated.

Original languageEnglish
Pages (from-to)1601-1618
Number of pages18
JournalJournal of Neurophysiology
Volume75
Issue number4
DOIs
Publication statusPublished - 1 Jan 1996

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