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 ORIGINAL ARTICLE
Year : 2018  |  Volume : 20  |  Issue : 97  |  Page : 223--231

Apoptosis in the cochlear nucleus and inferior colliculus upon repeated noise exposure


Department of Otolaryngology, Unfallkrankenhaus, Charité Medical School, Berlin, Germany

Correspondence Address:
Felix Frohlich
Research Scientist, Zentrum für klinische Technologieforschung, Warener Straße 7, Haus 49, 12683 Berlin
Germany
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/nah.NAH_30_18

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The time course of apoptosis and the corresponding neuronal loss was previously shown in central auditory pathway of mice after a single noise exposure. However, repeated acoustic exposure is a major risk factor for noise-induced hearing loss. The present study investigated apoptosis by terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling (TUNEL) assay after a second noise trauma in the ventral and dorsal cochlear nucleus and central nucleus of the inferior colliculus. Mice [Naval Medical Research Institute (NMRI) strain] were noise exposed [115 dB sound pressure level, 5–20 kHz, 3 h) at day 0. A double group received the identical noise exposure a second time at day 7 post-exposure and apoptosis was either analyzed immediately (7-day group-double) or 1 week later (14-day group-double). Corresponding single exposure groups were chosen as controls. No differences in TUNEL were seen between 7-day or 14-day single and double-trauma groups. Interestingly, independent of the second noise exposure, apoptosis increased significantly in the 14-day groups compared to the 7-day groups in all investigated areas. It seems that the first noise trauma has a long-lasting effect on apoptotic mechanisms in the central auditory pathway that were not largely influenced by a second trauma. Homeostatic mechanisms induced by the first trauma might protect the central auditory pathway from further damage during a specific time slot. These results might help to understand the underlying mechanisms of different psychoacoustic phenomena in noise-induced hearing loss.






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