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Synaptic Release Potentiation at Aging Auditory Ribbon Synapses
Age-related hidden hearing loss is often described as a cochlear synaptopathy that results from a progressive degeneration of the inner hair cell (IHC) ribbon synapses. The functional changes occurring at these synapses during aging are not fully understood. Here, we characterized this aging process...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8558230/ https://www.ncbi.nlm.nih.gov/pubmed/34733152 http://dx.doi.org/10.3389/fnagi.2021.756449 |
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author | Peineau, Thibault Belleudy, Séverin Pietropaolo, Susanna Bouleau, Yohan Dulon, Didier |
author_facet | Peineau, Thibault Belleudy, Séverin Pietropaolo, Susanna Bouleau, Yohan Dulon, Didier |
author_sort | Peineau, Thibault |
collection | PubMed |
description | Age-related hidden hearing loss is often described as a cochlear synaptopathy that results from a progressive degeneration of the inner hair cell (IHC) ribbon synapses. The functional changes occurring at these synapses during aging are not fully understood. Here, we characterized this aging process in IHCs of C57BL/6J mice, a strain which is known to carry a cadherin-23 mutation and experiences early hearing loss with age. These mice, while displaying a large increase in auditory brainstem thresholds due to 50% loss of IHC synaptic ribbons at middle age (postnatal day 365), paradoxically showed enhanced acoustic startle reflex suggesting a hyperacusis-like response. The auditory defect was associated with a large shrinkage of the IHCs' cell body and a drastic enlargement of their remaining presynaptic ribbons which were facing enlarged postsynaptic AMPAR clusters. Presynaptic Ca(2+) microdomains and the capacity of IHCs to sustain high rates of exocytosis were largely increased, while on the contrary the expression of the fast-repolarizing BK channels, known to negatively control transmitter release, was decreased. This age-related synaptic plasticity in IHCs suggested a functional potentiation of synaptic transmission at the surviving synapses, a process that could partially compensate the decrease in synapse number and underlie hyperacusis. |
format | Online Article Text |
id | pubmed-8558230 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-85582302021-11-02 Synaptic Release Potentiation at Aging Auditory Ribbon Synapses Peineau, Thibault Belleudy, Séverin Pietropaolo, Susanna Bouleau, Yohan Dulon, Didier Front Aging Neurosci Neuroscience Age-related hidden hearing loss is often described as a cochlear synaptopathy that results from a progressive degeneration of the inner hair cell (IHC) ribbon synapses. The functional changes occurring at these synapses during aging are not fully understood. Here, we characterized this aging process in IHCs of C57BL/6J mice, a strain which is known to carry a cadherin-23 mutation and experiences early hearing loss with age. These mice, while displaying a large increase in auditory brainstem thresholds due to 50% loss of IHC synaptic ribbons at middle age (postnatal day 365), paradoxically showed enhanced acoustic startle reflex suggesting a hyperacusis-like response. The auditory defect was associated with a large shrinkage of the IHCs' cell body and a drastic enlargement of their remaining presynaptic ribbons which were facing enlarged postsynaptic AMPAR clusters. Presynaptic Ca(2+) microdomains and the capacity of IHCs to sustain high rates of exocytosis were largely increased, while on the contrary the expression of the fast-repolarizing BK channels, known to negatively control transmitter release, was decreased. This age-related synaptic plasticity in IHCs suggested a functional potentiation of synaptic transmission at the surviving synapses, a process that could partially compensate the decrease in synapse number and underlie hyperacusis. Frontiers Media S.A. 2021-10-18 /pmc/articles/PMC8558230/ /pubmed/34733152 http://dx.doi.org/10.3389/fnagi.2021.756449 Text en Copyright © 2021 Peineau, Belleudy, Pietropaolo, Bouleau and Dulon. 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 | Neuroscience Peineau, Thibault Belleudy, Séverin Pietropaolo, Susanna Bouleau, Yohan Dulon, Didier Synaptic Release Potentiation at Aging Auditory Ribbon Synapses |
title | Synaptic Release Potentiation at Aging Auditory Ribbon Synapses |
title_full | Synaptic Release Potentiation at Aging Auditory Ribbon Synapses |
title_fullStr | Synaptic Release Potentiation at Aging Auditory Ribbon Synapses |
title_full_unstemmed | Synaptic Release Potentiation at Aging Auditory Ribbon Synapses |
title_short | Synaptic Release Potentiation at Aging Auditory Ribbon Synapses |
title_sort | synaptic release potentiation at aging auditory ribbon synapses |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8558230/ https://www.ncbi.nlm.nih.gov/pubmed/34733152 http://dx.doi.org/10.3389/fnagi.2021.756449 |
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