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J Neurophysiol (November 1, 2002). 10.1152/jn.00192.2002
Submitted on 15 March 2002
Accepted on 6 May 2002
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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