INVOLVEMENT OF COCHLEAR EFFERENT PATHWAYS IN PROTECTIVE EFFECTS ELICITED WITH BINAURAL LOUD SOUND EXPOSURE IN CATS. Rajan, R. Department of Psychology, Monash University, Clayton, Vic. 3168, Australia.
APStracts 2:0114N, 1995.
SUMMARY AND CONCLUSIONS
1. Studies in guinea pigs have shown that the crossed olivocochlear efferent (crossed OCB) pathways can reduce the cochlear neural desensitization caused by loud sounds. In one experimental paradigm, binaural loud sound exposure produced less damage than did monaural exposure, and various tests confirmed that this could be attributed to the OCB. In contrast, a study in cats has shown no such protection from the OCB for binaural exposures. There are some methodological differences between the cat and guinea pig studies which could account for the difference. The present study was carried out to determine if two factors, namely anaesthetic or exposure frequency, could account for the difference. Experiments were carried out in cats using barbiturate anaesthesia, as in the guinea pig experiments. 2. Using a unilateral MEM tenotomy it was confirmed that under Nembutal anaesthesia the MEM did not affect the threshold losses to monaural or binaural exposure. However, comparing results for monaural versus binaural 11 kHz exposures, there were significantly less threshold losses to the binaural exposure, independent of the presence of the MEM. No such difference between monaural and binaural exposures was seen for 3 kHz exposures. 3. By employing unilateral surgical strategies such as MEM tenotomy and/or various brainstem incisions it was confirmed that the protection with binaural compared to monaural 11 kHz exposure was due specifically to the OCB. In unilaterally de-efferented animals binaural 11 kHz exposure always produced lower threshold losses on the OCB-intact side than on the OCB-cut side, regardless of the status of the MEM. Brainstem cuts which affected other rostrally- or laterally-located structures but not the OCB produced similar threshold losses bilaterally after binaural exposure and the losses were comparable to the protected levels seen in other cases with intact OCB and binaural exposure. These data confirmed that when using an exposure frequency very similar to that used in the guinea pig experiments, a protective OCB effect could be demonstrated in cats as previously seen in guinea pigs. The MEM appeared to be inactive in barbiturate-anaesthetised animals and were not activated by 3, 7 or 11 kHz exposures at 100 dB SPL for 10 mins. The companion manuscript will demonstrate this same effect across a wider range of exposures. 4. Finally, across-group comparisons showed that binaural exposures at 11 kHz activated OCB-mediated protection while monaural exposures did not appear to do so and that, in this study in which the selection of animals for experimentation was tightly controlled, there was very good similarity in the threshold losses to the same exposure between groups in which the net theoretical outcome was the same. 

Received 19 September 1994; accepted in final form 17 March 1995.
APS Manuscript Number J589-4.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  1 May 1995.