Incomplete Recovery of Chicken Distortion Product Otoacoustic Emissions following Acoustic Overstimulation

Trautwein, Patricia G.; Salvi, Richard; Miller, Karen E.; Shero, Marlene; Hashino, Eri

doi:10.1159/000259188

Cited by 18 publications

(20 citation statements)

References 38 publications

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“…The maximum level reported here is approximately 10 dB higher than in our previous report since a higher current level was employed . As a point of comparison, the maximum EEOAE level is close to the maximum DPOAE that can be elicited from chickens using acoustic stimulation [Froymovich et al, 1995;Trautwein et al, 1996b]. The frequency response of our EEOAE had band pass characteristics with a peak near 3.5 kHz ( fig.…”

Section: Discussionsupporting

confidence: 54%

Acoustic Modulation of Electrically Evoked Otoacoustic Emission in Chickens

Sun

Chen²,

Salvi³

2002

Audiol Neurotol

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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.

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Section: Discussionsupporting

confidence: 54%

Acoustic Modulation of Electrically Evoked Otoacoustic Emission in Chickens

Sun

Chen²,

Salvi³

2002

Audiol Neurotol

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“…The effect of nonlinearity also appears in the compressive behavior of avian cochlear nerve rate-intensity functions (Richter et al 1995;KÖ ppl and Yates 1999;Yates et al 2000;Saunders et al 2002). In addition, acoustically or electrically evoked DPOAEs have provided another signature of nonlinear behavior (see, e.g., KÖ ppl 1995;Trautwein et al 1996;Chen et al 2001).…”

Section: Is the Stc A Proxy For Cochlear Mechanics?mentioning

confidence: 99%

Spatial Tuning Curves Along the Chick Basilar Papilla in Normal and Sound-Exposed Ears

Lifshitz

Furman

Altman

et al. 2004

JARO

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Intense sound exposure destroys chick short hair cells and damages the tectorial membrane. Within a few days postexposure, signs of repair appear resulting in nearly complete structural recovery of the inner ear. Tectorial membrane repair, however, is incomplete, leaving a permanent defect on the sensory surface. The consequences of this defect on cochlear function, and particularly frequency analysis, are unclear. The present study organizes the sound-induced discharge activity of cochlear nerve units to describe the distribution of neural activity along the tonotopic axis of the basilar papilla. The distribution of this activity is compared in 12-day postexposed and age-matched control groups. Spontaneous activity, tuning curves, and rate-intensity functions were measured in each unit. Discharge activity at 60 frequency and intensity combinations was identified in the tuning curves of hundreds of units. Activity at each of these criterion frequency/intensity combinations was plotted against the unit's characteristic frequency to construct spatial tuning curves (STCs). The STCs depict tone-driven cochlear nerve activity along the length of the papilla. Tuning sharpness, low-and high-frequency slopes, and the maximum response were quantified for each STC. The sharpness of tuning increased with increasing criterion frequency. However, within a frequency, increasing sound intensity yielded more broadly tuned STCs. Also, the high-frequency slope was consistently steeper than the low-frequency slope. The STCs of exposed ears exhibited slightly less frequency selectivity than control ears across all frequencies and larger maximum responses for STCs with criterion frequencies spanning the tectorial membrane defect. When rate-intensity types were segregated, differences were observed in the STCs between saturating and sloping-up units. We propose that STC shape may be determined by global mechanical events, as well as localized tuning and nonlinear processes associated with individual hair cells. The results indicated that 12 days after intense sound exposure, global and local contributions to spatially distributed neural activity are restored.

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“…Finally, the residual functional deficits observed after functional recovery from sound trauma correlate better with the area of the papilla over which recovery of the upper fibrous layer of the tectorial membrane was incomplete than with the area of lost and regenerated hair cells. This holds for DPOAEs [Froymovich et al, 1995;Trautwein et al, 1996b], behavioral temporal integration , pure-tone masking , TTRS Salvi et al, 1998] and the rateintensity functions of single auditory nerve fibers [Saunders et al, 1996a, b].…”

Section: Functional Regeneration and The Tectorial Membranementioning

confidence: 99%

“…This hypothesis was falsified, however, by the observation that, in adult chickens, the EP did not break down after sound trauma that caused severe global hearing loss at all frequencies . Thus although reduced EP, when it occurs, contributes to threshold elevation [Vossieck et al, 1991], other causes must be responsible for the global threshold elevation observed after sound trauma [Chen et al, 1996b, c;Trautwein et al, 1996bTrautwein et al, , 1997.…”

Section: Recovery Outside the Region Of Hair Cell Loss And Tectorial mentioning

confidence: 99%

Functional Recovery in the Avian Ear after Hair Cell Regeneration

Smolders

1999

Audiol Neurotol

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Trauma to the inner ear in birds, due to acoustic overstimulation or ototoxic aminoglycosides, can lead to hair cell loss which is followed by regeneration of new hair cells. These processes are paralleled by hearing loss followed by significant functional recovery. After acoustic trauma, functional recovery is rapid and nearly complete. The early and major part of functional recovery after sound trauma occurs before regenerated hair cells become functional. Even very intense sound trauma causes loss of only a proportion of the hair cell popu- lation, mainly so-called short hair cells residing on the abneural mobile part of the avian basilar membrane. Uncoupling of the tectorial membrane from the hair cells during sound overexposure may serve as a protection mechanism. The rapid functional recovery after sound trauma appears not to be associated with regeneration of the lost hair cells, but with repair processes involving the surviving hair cells. Small residual functional deficits after recovery are most likely associated with the missing upper fibrous layer of the tectorial membrane which fails to regenerate after sound trauma. After aminoglycoside trauma, functional recovery is slower and parallels the structural regeneration more closely. Aminoglycosides cause damage to both types of hair cells, starting at the basal (high frequency) part of the basilar papilla. However, functional hearing loss and recovery also occur at lower frequencies, associated with areas of the papilla where hair cells survive. Functional recovery in these low frequency areas is complete, whereas functional recovery in high frequency areas with complete hair cell loss is incomplete, despite regeneration of the hair cells. Permanent residual functional deficits remain. This indicates that in low frequency regions functional recovery after aminoglycosides involves repair of nonlethal injury to hair cells and/or hair cell-neural synapses. In the high frequency regions functional recovery involves regenerated hair cells. The permanent functional deficits after the regeneration process in these areas are most likely associated with functional deficits in the regenerated hair cells or shortcomings in the synaptic reconnections of nerve fibers with the regenerated hair cells. In conclusion, the avian inner ear appears to be much more resistant to trauma than the mammalian ear and possesses a considerable capacity for functional recovery based on repair processes along with its capacity to regenerate hair cells. The functional recovery in areas with regenerated hair cells is considerable but incomplete.

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Incomplete Recovery of Chicken Distortion Product Otoacoustic Emissions following Acoustic Overstimulation

Cited by 18 publications

References 38 publications

Acoustic Modulation of Electrically Evoked Otoacoustic Emission in Chickens

Acoustic Modulation of Electrically Evoked Otoacoustic Emission in Chickens

Spatial Tuning Curves Along the Chick Basilar Papilla in Normal and Sound-Exposed Ears

Functional Recovery in the Avian Ear after Hair Cell Regeneration

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