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Year : 2017  |  Volume : 19  |  Issue : 88  |  Page : 133--139

Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex

Department of Otolaryngology, Unfallkrankenhaus Berlin, Charité Medical School, Warener Straß 7, Berlin, Germany

Correspondence Address:
Moritz Gröschel
Department of Otolaryngology, Unfallkrankenhaus Berlin, Charité Medical School, Warener Straß 7, 12683 Berlin
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/nah.NAH_10_17

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It has previously been shown that acoustic overstimulation induces cell death and extensive cell loss in key structures of the central auditory pathway. A correlation between noise-induced apoptosis and cell loss was hypothesized for the cochlear nucleus and colliculus inferior. To determine the role of cell death in noise-induced cell loss in thalamic and cortical structures, the present mouse study (NMRI strain) describes the time course following noise exposure of cell death mechanisms for the ventral medial geniculate body (vMGB), medial MGB (mMGB), and dorsal MGB (dMGB) and the six histological layers of the primary auditory cortex (AI 1–6). Therefore, a terminal deoxynucleotidyl transferase dioxyuridine triphosphate nick-end labeling assay (TUNEL) was performed in these structures 24 h, 7 days, and 14 days after noise exposure (3 h, 115 dB sound pressure level, 5–20 kHz), as well as in unexposed controls. In the dMGB, TUNEL was statistically significant elevated 24 h postexposure. AI-1 showed a decrease in TUNEL after 14 days. There was no statistically significant difference between groups for the other brain areas investigated. dMGB’s widespread connection within the central auditory pathway and its nontonotopical organization might explain its prominent increase in TUNEL compared to the other MGB subdivisions and the AI. It is assumed that the onset and peak of noise-induced cell death is delayed in higher areas of the central auditory pathway and takes place between 24 h and 7 days postexposure in thalamic and cortical structures.


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