ADDITIVITY OF LOUD-SOUND-INDUCED THRESHOLD LOSSES IN THE CAT UNDER
CONDITIONS OF ACTIVE OR INACTIVE COCHLEAR EFFERENT-MEDIATED PROTECTION.
Rajan, R.
Department of Psychology, Monash University, Clayton, Vic. 3168,
Australia.
APStracts 2:0312N, 1995.
SUMMARY AND CONCLUSIONS
1. An additivity model for the accretion of cochlear sensorineural hearing
losses has been described from studies in the guinea pig cochlea (Patuzzi and
Rajan, 1992). 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 3-15 kHz, affecting regions from 2-28 kHz.
Successive identical exposures, generally with an inter-exposure interval of
nearly equal to 35 mins, were used to produce compound action potential (CAP)
threshold losses. Total losses after E2 were compared to those predicted by
the model. Testing was carried out under conditions where olivocochlear bundle
(OCB) - mediated protection (Rajan, 1992, 1995a, b) was or was not activated.
(As shown elsewhere (Rajan, 1995a, b), 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 to losses in either
the monaural condition, or the binaural condition where the OCB was cut prior
to 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 databases 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 (Rajan, 1995b) and guinea pig
(Rajan, 1988b; Rajan and Johnstone, 1988a). 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 (Rajan, 1995a). 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.
Received 26 May 1995; accepted in final form 23 October 1995.
APS Manuscript Number J346-5.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 6 November 95