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Investigation of noise-induced degeneration of efferent nerve fibers in the mammalian inner ear as cause of hyperacusis

Subject Area Otolaryngology, Phoniatrics and Audiology
Term from 2018 to 2024
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 413271458
 
Too high sound pressure levels can be perceived as pain. This usually occurs above a level of 120 dB SPL. If this is clearly below this level, one speaks of a hyperacusis. This hypersensitivity to sound is probably due to damage to structures in the inner ear. In the inner ear of mammals neuronal signals, which are forwarded to the brain, are generated in an extremely complex interplay between inner ear mechanics and efferent control. In the present project, we will investigate, besides the changes in the afferent connections, whether the degeneration of efferent connections after a noise trauma causes a change in the neuronal activity of the afferents and is thus a cause of hyperacusis? In the inner ear of mammals, there are two types of sense cells, the inner hair cells and the outer hair cells (OHC). The OHC have piezoelectric properties (electromotility), which can amplify the mechanical signal at low sound pressure levels or attenuate the mechanical signal at high sound pressure levels. The OHCs are thus involved in the extremely sensitive hearing in mammals and contribute to the protection of the hearing function when the sound pressure is too high. The piezoelectricity of the OHCs at high sound pressure levels is reduced by means of efferents, which are connected to the basal pol of the OHC. A loss of these nerve fibers by a noise trauma could disturb this protective mechanism and have far-reaching consequences, including the development of hyperacusis. Using monaural-evoked brain stem potentials and otoacoustic emissions (f2-f1), we will investigate the possible degeneration of efferent nerve fibers and their effects on neuronal processing in young and old Mongolian gerbil. In these experiments, the efferent system is activated by a contralateral noise, whereby we will test the influence of this activation before and after the noise trauma. In addition, we will document the stress values of the animals in order to correlate the mechanical and neurophysiological data with the behavioral studies on the startle reflex, which will provide us information about the development of hyperacusis. Finally, the extent of degeneration and regeneration of the efferent fibers in the inner ear will be determined by fiber staining. Taking into account the age of the animals, we hope to understand better through these comprehensive mechanical, neurophysiological and behavioral studies of noise-induced damage the mechanisms of development of hyperacusis and to provide a basis for the development of treatment methods.
DFG Programme Research Grants
 
 

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