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

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 rol...

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Autores principales: Fröhlich, Felix, Basta, Dietmar, Strübing, Ira, Ernst, Arne, Gröschel, Moritz
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5501023/
https://www.ncbi.nlm.nih.gov/pubmed/28615543
http://dx.doi.org/10.4103/nah.NAH_10_17
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author Fröhlich, Felix
Basta, Dietmar
Strübing, Ira
Ernst, Arne
Gröschel, Moritz
author_facet Fröhlich, Felix
Basta, Dietmar
Strübing, Ira
Ernst, Arne
Gröschel, Moritz
author_sort Fröhlich, Felix
collection PubMed
description 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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spelling pubmed-55010232017-07-13 Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex Fröhlich, Felix Basta, Dietmar Strübing, Ira Ernst, Arne Gröschel, Moritz Noise Health Original Article 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. Medknow Publications & Media Pvt Ltd 2017 /pmc/articles/PMC5501023/ /pubmed/28615543 http://dx.doi.org/10.4103/nah.NAH_10_17 Text en Copyright: © 2017 Noise & Health http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
spellingShingle Original Article
Fröhlich, Felix
Basta, Dietmar
Strübing, Ira
Ernst, Arne
Gröschel, Moritz
Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex
title Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex
title_full Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex
title_fullStr Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex
title_full_unstemmed Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex
title_short Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex
title_sort time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5501023/
https://www.ncbi.nlm.nih.gov/pubmed/28615543
http://dx.doi.org/10.4103/nah.NAH_10_17
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