EFFECTS OF KAINIC ACID ON THE COCHLEAR POTENTIALS AND DISTORTION-PRODUCT OTOACOUSTIC EMISSIONS IN CHINCHILLA

In absence of acoustic stimulation, the auditory nerve generates elect rical noise with a spectral peak between 300 and 3000 Hz (Dolan et al. , 1990). This electrical noise is eliminated when the dendrites of aud itory nerve fibers are damaged by kainic acid (KA). We hypothesized th at the KA-induced damage to the afferent dendrites might alter cochlea r micromechanics or modify outer hair cell (OHC) electromotility. The KA-induced decrease in spontaneous electrical noise from the auditory nerve could conceivably reduce the spontaneous sounds recorded in the ear canal and the postulated change in cochlear micromechanics might a lter distortion product otoacoustic emissions (DPOAE). To evaluate the se hypotheses, we applied KA to the round window of the cochlea. KA re duced the spontaneous electrical noise recorded from the round window and significantly reduced the amplitude of the compound action potenti al (CAP) to tone bursts at 2, 4 and 8 kHz. KA caused only a slight red uction in the amplitude of the cochlear microphonic (CM) recorded from the round window; however, it had no effect on the spontaneous acoust ic noise in the ear canal or on 2fl-f2 DPOAEs. These results suggest t hat the KA-induced reduction of electrical noise from the auditory ner ve has no measurable effect on OHC electromotility as reflected in spo ntaneous otoacoustic emissions and that damage to the afferent dendrit es has no effect on cochlear micromechanics as reflected in DPOAEs.