FREQUENCY- AND LOSS-DEPENDENCE OF THE PROTECTIVE EFFECTS OF THE OLIVOCOCHLEAR PATHWAYS IN CATS. Rajan, R. Department of Psychology, Monash University, Clayton, Vic. 3168, Australia.
APStracts 2:0115N, 1995.
SUMMARY AND CONCLUSIONS
1. The previous manuscript suggested a frequency-dependency to OCB-mediated protection from loud sound by showing protection for binaural compared to monaural 11 kHz exposures but not 3 kHz exposures at the same intensity and for the same duration. To determine if this was the case, experiments were carried out in barbiturate-anaesthetized cats using the paradigm of a unilateral brainstem incision to de-efferent one cochlea in each animal before presenting a binaural loud sound exposure. With equi-intensity, equi-duration binaural exposures, in different groups protection in OCB-intact compared to OCB-cut ears was seen only for exposures at 11, 15 or 20 kHz, but not at 3 or 7 kHz, suggesting that OCB-mediated protection was found only for higher frequency exposures. This would be consistent with the OCB-mediated protection in guinea-pig studies using 10 kHz exposures and it's absence in a study in cats (Liberman, 1991) using 6 kHz exposures. However, this conclusion had to be qualified by the fact that the lower frequency exposures resulted in smaller threshold losses than did the higher frequency exposures. 2. To determine if OCB-mediated protection could be obtained for lower-frequency exposures that were made as damaging as or more damaging than the high frequency exposures, longer-duration lower-frequency exposures were used. OCB- mediated protection could then be obtained for exposure at 7 kHz 100 dB SPL for 15 mins but not at 3 or 5 kHz at 100 dB SPL for 20 mins, or at 3 kHz 100 dB SPL for 40 mins or 106 dB SPL for 20 mins. Finally when large threshold losses were produced with exposure at 3 kHz 106 dB SPL for 40 mins, OCB- mediated protection could be obtained for this low frequency exposure too. These effects suggested that there were different "activation thresholds" for OCB-mediated protection as a function of exposure frequency. To determine if this also applied for the higher frequency exposures (11, 15 and 20 kHz) all of which had elicited OCB-mediated protection when presented at 100 dB SPL for 10 mins, these exposure frequencies were presented at 100 dB SPL for 7 mins to produce low threshold losses. Now protection was found for the 11 and 15 kHz exposures but not for the 20 kHz exposure. 3. Thus, the "activation threshold" for OCB-mediated protection varied in a frequency-dependent manner. When the different exposures were "titrated" to compare conditions producing similar threshold losses, for low-damage exposures protection was obtained only for 11 and 15 kHz exposures, for moderately-damaging exposures protection extended to higher but not lower frequencies, and finally, for severely-damaging exposures all exposure frequencies from 3-20 kHz elicited protection. Post-hoc analysis revealed that this variation in "activation threshold" for OCB-mediated protection could be related to normal hearing sensitivity at the cochlea, as assessed by the compound action potential audiogram, and to the damaging capacity of different exposure frequencies. 4. The brainstem incision used thus far did not differentiate between different components of the OCB. To determine the involvement of specific OCB sub-sets in protection, brainstem cuts were placed to cut the entire OCB to one cochlea and only the COCB to the other cochlea prior to a binaural high-frequency exposure. Data from this group showed that the COCB was critically involved in the OCB-mediated protection. 5. An inference from earlier analyses was that monaural exposures did not activate OCB-mediated protection. Testing with consecutive monaural exposure to the two ears in a group in which the OCB had been cut to only one ear explicitly confirmed that monaural exposure did not suffice to activate protection in these barbiturate-anaesthetised cats. 6. Finally, although the "activation threshold" for protection varied with exposure frequency, for all exposure frequencies once this "threshold" had been exceeded there was a strong linear relationship between the amount of protection and the threshold loss that would otherwise occur. When the relationship for 11 kHz exposures in cats in this study was compared to that seen for 10 kHz exposures in previous studies in guinea pigs, there was very good similarity, showing the generality of this relationship across the two species, for similar exposure frequencies. 

Received 19 September 1994; accepted in final form 17 March 1995.
APS Manuscript Number J590-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  1 May 1995.