Acoustic Modulation of Electrically Evoked Otoacoustic Emission in Chickens

Abstract

Electrically evoked otoacoustic emissions (EEOAEs) can be elicited from the chicken inner ear. Since lesion studies implicate hair cells are the source of EEOAEs, we hypothesized that acoustic stimuli would modulate EEOAE amplitude at cochlear locations where the acoustic and electrical stimuli overlap. To assess this interaction, EEOAEs were measured as the frequency and amplitude of the acoustic stimuli were varied. EEOAEs, evoked by AC current (3–250 µA rms) delivered to the round window had a broad band pass response (1–6 kHz) with a peak between 3 and 4 kHz and maximum amplitude of 27 dB SPL. EEOAE suppression/enhancement tuning curves were measured at 2, 3, 4 and 6 kHz by varying the frequency of a 70 dB SPL tone and measuring the change in EEOAE amplitude. EEOAE tuning curves were characterized by a tip; a narrow range of frequencies where EEOAE amplitude was suppressed by as much as 5 dB, and by sidebands, a range of frequencies above and below the tip where EEOAE amplitude was enhanced by as much as 1.5 dB. The best suppression frequency, or characteristic frequency, was close to the frequency of the EEOAE elicited by the 3- or 4-kHz electric stimulus. However, the characteristic frequency was displaced towards higher frequencies for the 2-kHz electric stimulus, and towards lower frequencies for the 6-kHz electric stimulus. EEOAE suppression increased approximately linearly with acoustic level. These results suggest that EEOAEs evoked by round window stimulation are predominantly generated by hair cells near the 3- to 4-kHz region of the cochlea.

Return of function after hair cell regeneration

“…Other less direct measures of regenerated hair cell viability, such as the cochlear microphonic and distortion product otoacoustic emissions, have also shown some return of function following regeneration (see Saunders and Salvi, 2008 for review). The cochlear microphonic shows substantial but incomplete recovery 11–14 weeks after ototoxic injury and hair cell regeneration (Chen et al 2001; Sun et al 2002), confirming recovery of transduction currents in regenerated hair cells. Distortion product otoacoustic emission (DPOAE) thresholds, input-output responses and amplitudes show partial to full recovery with the most consistent lingering decline at the highest frequencies (Chen et al 2001; Norton and Rubel, 1990; Durham et al 2000).…”