Effects of kainic acid on the cochlear potentials and distortion product otoacoustic emissions in chinchilla.

In absence of acoustic stimulation, the auditory nerve generates electrical noise with a spectral peak between 300 and 3000 Hz (Dolan et al., 1990). This electrical noise is eliminated when the dendrites of auditory nerve fibers are damaged by kainic acid (KA). We hypothesized that the KA-induced damage to the afferent dendrites might alter cochlear 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 alter distortion product otoacoustic emissions (DPOAE). To evaluate these hypotheses, we applied KA to the round window of the cochlea. KA reduced the spontaneous electrical noise recorded from the round window and significantly reduced the amplitude of the compound action potential (CAP) to tone bursts at 2, 4 and 8 kHz. KA caused only a slight reduction in the amplitude of the cochlear microphonic (CM) recorded from the round window: however, it had no effect on the spontaneous acoustic noise in the car canal or on 2 f1-f2 DPOAEs. These results suggest that the KA-induced reduction of electrical noise from the auditory nerve has no measurable effect on OHC electromotility as reflected in spontaneous otoacoustic emissions and that damage to the afferent dendrites has no effect on cochlear micromechanics as reflected in DPOAEs.