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J Neurophysiol 91: 784-795, 2004. First published October 8, 2003; doi:10.1152/jn.00776.2003
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Response Growth With Sound Level in Auditory-Nerve Fibers After Noise-Induced Hearing Loss

Michael G. Heinz and Eric D. Young

Center for Hearing Sciences and Department of Biomedical Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Submitted 11 August 2003; accepted in final form 3 October 2003

People with sensorineural hearing loss are often constrained by a reduced acoustic dynamic range associated with loudness recruitment; however, the neural correlates of loudness and recruitment are still not well understood. The growth of auditory-nerve (AN) activity with sound level was compared in normal-hearing cats and in cats with a noise-induced hearing loss to test the hypothesis that AN-fiber rate-level functions are steeper in impaired ears. Stimuli included best-frequency and fixed-frequency tones, broadband noise, and a brief speech token. Three types of impaired responses were observed. 1) Fibers with rate-level functions that were similar across all stimuli typically had broad tuning, consistent with outer-hair-cell (OHC) damage. 2) Fibers with a wide dynamic range and shallow slope above threshold often retained sharp tuning, consistent with primarily inner-hair-cell (IHC) damage. 3) Fibers with very steep rate-level functions for all stimuli had thresholds above approximately 80 dB SPL and very broad tuning, consistent with severe IHC and OHC damage. Impaired rate-level slopes were on average shallower than normal for tones, and were steeper in only limited conditions. There was less variation in rate-level slopes across stimuli in impaired fibers, presumably attributable to the lack of suppression-induced reductions in slopes for complex stimuli relative to BF-tone slopes. Sloping saturation was observed less often in impaired fibers. These results illustrate that AN fibers do not provide a simple representation of the basilar-membrane I/O function and suggest that both OHC and IHC damage can affect AN response growth.


Address for reprint requests and other correspondence: M. G. Heinz, Department of Biomedical Engineering, 505 Traylor Building, Johns Hopkins University, 720 Rutland Avenue, Baltimore, MD 21205 (E-mail: mgheinz{at}bme.jhu.edu).




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