Open AccessApoptosis in the cochlear nucleus and inferior colliculus upon repeated noise exposure
Author(s) -
Felix Fröhlich,
Moritz Gröschel,
Ira Strübing,
Arne Ernst,
Dietmar Basta
Publication year - 2018
Publication title -
noise and health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.344
H-Index - 48
eISSN - 1998-4030
pISSN - 1463-1741
DOI - 10.4103/nah.nah_30_18
Subject(s) - inferior colliculus , tunel assay , noise induced hearing loss , apoptosis , terminal deoxynucleotidyl transferase , cochlear nucleus , hearing loss , noise (video) , presbycusis , medicine , audiology , neuroscience , endocrinology , chemistry , biology , anesthesia , noise exposure , nucleus , biochemistry , artificial intelligence , computer science , image (mathematics)
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.