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Noise-induced focal lesions in the Organ of Corti: distribution and cell-death pathways.
Abstr 32nd Midwinter Res Meet 2009 Feb; 32:47
Studies have been conducted to identify what death pathways OHCs follow after moderate-severe noise exposures. Identified pathways include oncosis/necrosis, apoptosis & a non-apoptotic, non-oncotic pathway. IHCs, pillar & Deiters cells are also destroyed by noise. In order to develop treatment strategies that will minimize noise-induced hearing loss, it is important to identify death pathways in all cell types in the organ of Corti (OC). Eighteen chinchillas were exposed for 1 h to a 4-kHz OBN at 108 dB SPL. Recovery times were < 1 d to 30 d post-exposure. At termination, animals were anesthetized; their cochleae surgically exposed & fixed in-vivo with 1% buffered OsO4. The intact cochleae were dehydrated, embedded in plastic & dissected into flat preparations. For each ear, OC length was measured & losses of cells were quantified throughout the OC. Focal hair-cell lesions were identified [= 50% loss of OHCs, IHCs or both (i.e., combined) over at least 0.03 mm] and death pathways in dying cells determined. All but one cochlea had one or more focal hair-cell lesions. In different cochleae, some lesions covered a narrow portion of the OC & were close to the 4-kHz OBN location, while some lesions were spread over approximately 50% of the OC. In cochleae with two or more lesions, variable-length areas of reduced damage separated the lesions. Twice as many OHC lesions as combined & IHC lesions were identified. OHC & combined lesions were greater in length than IHC lesions & usually included missing pillars & Deiters cells. IHC lesions rarely involved other cell types. This suggests that IHC lesions are generated by a different mechanism than OHC & combined lesions. Within the OHC & combined focal lesions, dying hair cells were identified that were following the oncotic, apoptotic & non-apoptotic, non-oncotic death pathways. The identification of death pathways followed by IHCs in IHC focal lesions & by supporting cells in OHC & combined focal lesions is in progress.
Noise-exposure; Exposure-levels; Noise-induced-hearing-loss; Noise-exposure; Noise; Hearing; Hearing-disorders; Hearing-loss; Laboratory-animals; Animals
Barbara A. Bohne, Ph.D., Washington University School of Medicine, Dept. of Otolaryngology, Box 8115, 660 South Euclid A venue, St. Louis, MO 63110
Abstracts of the 32nd Midwinter Research Meeting
Washington University, St. Louis
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