Suppression and enhancement of distortion-product otoacoustic emissions by interference tones above f(2). I. Basic findings in rabbits.

The present study measured interference-response areas (IRAs) for distortion-product otoacoustic emissions (DPOAEs) at 2f(1)-f(2), 3f(1)-2f(2), and 2f(2)-f(1). The IRAs were obtained in either awake or anesthetized rabbits, or in anesthetized guinea pigs and mice, by sweeping the frequencies and levels of an interference tone (IT) around a set of f(1) and f(2) primary tones, at several fixed frequencies and levels, while plotting the effects of the IT on DPOAE level. An unexpected outcome was the occurrence of regions of suppression and/or enhancement of DPOAE level when the IT was at a frequency slightly less than to more than an octave above f(2). The IRA of the 2f(1)-f(2) DPOAE typically displayed a high-frequency (HF) lobe of suppression, while the 2f(2)-f(1) emission often exhibited considerable amounts of enhancement. Moreover, for the 2f(2)-f(1) DPOAE, when enhancement was absent, its IRA usually tuned to a region above f(2). Whether or not suppression/enhancement was observed depended upon primary-tone level and frequency separation, as well as on the relative levels of the two primaries. Various physiological manipulations involving anesthesia, eighth-nerve section, diuretic administration, or pure-tone overstimulation showed that these phenomena were of cochlear origin, and were not dependent upon the acoustic reflex or cochlear-efferent activity. The aftereffects of applying diuretics or over-exposures revealed that suppression/enhancement required the presence of sensitive, low-level DPOAE-generator sources. Additionally, suppression/enhancement were general effects in that, in addition to rabbits, they were also observed in mice and guinea pigs. Further, corresponding plots of DPOAE phase often revealed areas of differing phase change in the vicinity of the primary tones as compared to regions above f(2). These findings, along with the effects of tonal exposures designed to fatigue regions above f(2), and instances in which DPOAE level was dependent upon the amount of suppression/enhancement, suggested that the interactions of two DPOAE-generator sources contributed, in some manner, to these phenomena.