Despite over 100 years of experimental research, our understanding of the mechanisms underlying noise trauma, or the means of protecting against noise trauma, needs to be clarified. Protection against noise trauma has been demonstrated recently by sound conditioning guinea pigs to a low level, long term acoustic stimulus (Canlon et al. 1988). This sound conditioning ameliorated the damaging effects of a second noise exposure that was expected to yield a permanent hearing loss. The sound conditioned group showed complete recovery, while the control group continued to show a 20 to 30 dB permanent hearing loss. These findings are not particular to the guinea pig, since preliminary results indicate that the rabbit responds to sound conditioning in the same fashion. The sound conditioning experiments originated from current concepts of auditory physiology which include active cellular mechanisms. Since the finding that the outer hair cells have a motile capacity, it has been suggested, that they are the active elements. It was proposed that sound conditioning would enhance a muscle-like capacity of the outer hair cells (Canlon et al. 1988). Preliminary morphological findings imply that sound conditioning improves the metabolic capacity of the outer hair cells. As a result of these exciting phenomena, numerous studies will be pursued in order to test our hypothesis that the intrinsic properties of the outer hair cells are directly affected by sound conditioning. A battery of readily available and established electrophysiological and morphological tests can be applied to obtain specific information concerning the outer hair cells. The following specific aims will be addressed: (1) To determine if sound conditioning results in (i) an altered morphology to the organ of Corti; (ii) an altered pattern of damage after subsequent noise exposure. (2) To measure outer hair cell resistance after sound conditioning by analyzing the magnitude of a temporary threshold shift and the rate of recovery of the cubic distortion product (2fl-f2). (3) To determine how sound conditioning preserves the frequency selectivity of the auditory system. (4) To determine what features of the conditioning stimulus are necessary for noise protection. (5) To determine if the efferent system plays a role in sound conditioning. (6) To determine if the middle ear muscles regulate sound conditioning. (7) To quantify how sound conditioning modifies the intrinsic biological properties of the hair cells. This research will be of importance not only in understanding cochlear mechanisms but also in developing a deeper understanding of noise trauma and how it may be possibly reduced.

Agency
National Institute of Health (NIH)
Institute
National Institute on Deafness and Other Communication Disorders (NIDCD)
Type
Research Project (R01)
Project #
5R01DC001403-03
Application #
2126476
Study Section
Hearing Research Study Section (HAR)
Project Start
1992-07-01
Project End
1995-06-30
Budget Start
1994-07-01
Budget End
1995-06-30
Support Year
3
Fiscal Year
1994
Total Cost
Indirect Cost
Name
Karolinska Institute
Department
Type
DUNS #
350582235
City
Stockholm
State
Country
Sweden
Zip Code
171 7-7
Fowler, T; Canlon, B; Dolan, D et al. (1995) The effect of noise trauma following training exposures in the mouse. Hear Res 88:1-13