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J Neurophysiol 88: 2341-2348, 2002; doi:10.1152/jn.00192.2002
0022-3077/02 $5.00
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J Neurophysiol (November 1, 2002). 10.1152/jn.00192.2002
Submitted on 15 March 2002
Accepted on 6 May 2002

Loud Sound-Induced Changes in Cochlear Mechanics

Anders Fridberger,5 Jiefu Zheng,1,3 Anand Parthasarathi,4 Tianying Ren,1 and Alfred Nuttall1,2

 1Oregon Hearing Research Center, Department of Otolaryngology/Head and Neck Surgery, Oregon Health & Science University, Portland, Oregon 97239;  2Kresge Hearing Research Institute, The University of Michigan, Ann Arbor, Michigan, 48109-0506;  3Department of Otolaryngology, Chinese PLA General Hospital, Beijing 100853, P.R. China;  4Bose Corporation, Framingham, Massachusetts 01701; and  5Karolinska Institutet, Department of Physiology and Pharmacology, SE-171 77 Stockholm, Sweden

Fridberger, Anders, Jiefu Zheng, Anand Parthasarathi, Tianying Ren, and Alfred Nuttall. Loud Sound-Induced Changes in Cochlear Mechanics. J. Neurophysiol. 88: 2341-2348, 2002. To investigate the inner ear response to intense sound and the mechanisms behind temporary threshold shifts, anesthetized guinea pigs were exposed to tones at 100-112 dB SPL. Basilar membrane vibration was measured using laser velocimetry, and the cochlear microphonic potential, compound action potential of the auditory nerve, and local electric AC potentials in the organ of Corti were used as additional indicators of cochlear function. After exposure to a 12-kHz intense tone, basilar membrane vibrations in response to probe tones at the characteristic frequency of the recording location (17 kHz) were transiently reduced. This reduction recovered over the course of 50 ms in most cases. Organ of Corti AC potentials were also reduced and recovered with a time course similar to the basilar membrane. When using a probe tone at either 1 or 4 kHz, organ of Corti AC potentials were unaffected by loud sound, indicating that transducer channels remained intact. In most experiments, both the basilar membrane and the cochlear microphonic response to the 12-kHz overstimulation was constant throughout the duration of the intense stimulus, despite a large loss of cochlear sensitivity. It is concluded that the reduction of basilar membrane velocity that followed loud sound was caused by changes in cochlear amplification and that the cochlear response to intense stimulation is determined by the passive mechanical properties of the inner ear structures.




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