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Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure

After acoustic trauma, there can be loss of synaptic connections between inner hair cells and auditory neurons in the cochlea, which may lead to hearing abnormalities including speech-in-noise difficulties, tinnitus, and hyperacusis. We have previously studied mice with blast-induced cochlear synapt...

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Autores principales: Badash, Ido, Quiñones, Patricia M., Oghalai, Kevin J., Wang, Juemei, Lui, Christopher G., Macias-Escriva, Frank, Applegate, Brian E., Oghalai, John S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8602199/
https://www.ncbi.nlm.nih.gov/pubmed/34805158
http://dx.doi.org/10.3389/fcell.2021.747870
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author Badash, Ido
Quiñones, Patricia M.
Oghalai, Kevin J.
Wang, Juemei
Lui, Christopher G.
Macias-Escriva, Frank
Applegate, Brian E.
Oghalai, John S.
author_facet Badash, Ido
Quiñones, Patricia M.
Oghalai, Kevin J.
Wang, Juemei
Lui, Christopher G.
Macias-Escriva, Frank
Applegate, Brian E.
Oghalai, John S.
author_sort Badash, Ido
collection PubMed
description After acoustic trauma, there can be loss of synaptic connections between inner hair cells and auditory neurons in the cochlea, which may lead to hearing abnormalities including speech-in-noise difficulties, tinnitus, and hyperacusis. We have previously studied mice with blast-induced cochlear synaptopathy and found that they also developed a build-up of endolymph, termed endolymphatic hydrops. In this study, we used optical coherence tomography to measure endolymph volume in live CBA/CaJ mice exposed to various noise intensities. We quantified the number of synaptic ribbons and postsynaptic densities under the inner hair cells 1 week after noise exposure to determine if they correlated with acute changes in endolymph volume measured in the hours after the noise exposure. After 2 h of noise at an intensity of 95 dB SPL or below, both endolymph volume and synaptic counts remained normal. After exposure to 2 h of 100 dB SPL noise, mice developed endolymphatic hydrops and had reduced synaptic counts in the basal and middle regions of the cochlea. Furthermore, round-window application of hypertonic saline reduced the degree of endolymphatic hydrops that developed after 100 dB SPL noise exposure and partially prevented the reduction in synaptic counts in the cochlear base. Taken together, these results indicate that endolymphatic hydrops correlates with noise-induced cochlear synaptopathy, suggesting that these two pathologic findings have a common mechanistic basis.
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spelling pubmed-86021992021-11-20 Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure Badash, Ido Quiñones, Patricia M. Oghalai, Kevin J. Wang, Juemei Lui, Christopher G. Macias-Escriva, Frank Applegate, Brian E. Oghalai, John S. Front Cell Dev Biol Cell and Developmental Biology After acoustic trauma, there can be loss of synaptic connections between inner hair cells and auditory neurons in the cochlea, which may lead to hearing abnormalities including speech-in-noise difficulties, tinnitus, and hyperacusis. We have previously studied mice with blast-induced cochlear synaptopathy and found that they also developed a build-up of endolymph, termed endolymphatic hydrops. In this study, we used optical coherence tomography to measure endolymph volume in live CBA/CaJ mice exposed to various noise intensities. We quantified the number of synaptic ribbons and postsynaptic densities under the inner hair cells 1 week after noise exposure to determine if they correlated with acute changes in endolymph volume measured in the hours after the noise exposure. After 2 h of noise at an intensity of 95 dB SPL or below, both endolymph volume and synaptic counts remained normal. After exposure to 2 h of 100 dB SPL noise, mice developed endolymphatic hydrops and had reduced synaptic counts in the basal and middle regions of the cochlea. Furthermore, round-window application of hypertonic saline reduced the degree of endolymphatic hydrops that developed after 100 dB SPL noise exposure and partially prevented the reduction in synaptic counts in the cochlear base. Taken together, these results indicate that endolymphatic hydrops correlates with noise-induced cochlear synaptopathy, suggesting that these two pathologic findings have a common mechanistic basis. Frontiers Media S.A. 2021-11-05 /pmc/articles/PMC8602199/ /pubmed/34805158 http://dx.doi.org/10.3389/fcell.2021.747870 Text en Copyright © 2021 Badash, Quiñones, Oghalai, Wang, Lui, Macias-Escriva, Applegate and Oghalai. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Cell and Developmental Biology
Badash, Ido
Quiñones, Patricia M.
Oghalai, Kevin J.
Wang, Juemei
Lui, Christopher G.
Macias-Escriva, Frank
Applegate, Brian E.
Oghalai, John S.
Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure
title Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure
title_full Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure
title_fullStr Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure
title_full_unstemmed Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure
title_short Endolymphatic Hydrops is a Marker of Synaptopathy Following Traumatic Noise Exposure
title_sort endolymphatic hydrops is a marker of synaptopathy following traumatic noise exposure
topic Cell and Developmental Biology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8602199/
https://www.ncbi.nlm.nih.gov/pubmed/34805158
http://dx.doi.org/10.3389/fcell.2021.747870
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