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Mechanisms contributing to central excitability changes during hearing loss

Exposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America 22 May 2012, Vol.109(21), pp.8292-7
Main Author: Pilati, Nadia
Other Authors: Ison, Matias J , Barker, Matthew , Mulheran, Mike , Large, Charles H , Forsythe, Ian D , Matthias, John , Hamann, Martine
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1091-6490 ; PMID: 22566618 Version:1 ; DOI: 10.1073/pnas.1116981109
Link: http://pubmed.gov/22566618
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recordid: medline22566618
title: Mechanisms contributing to central excitability changes during hearing loss
format: Article
creator:
  • Pilati, Nadia
  • Ison, Matias J
  • Barker, Matthew
  • Mulheran, Mike
  • Large, Charles H
  • Forsythe, Ian D
  • Matthias, John
  • Hamann, Martine
subjects:
  • Cochlear Nerve -- Physiopathology
  • Cochlear Nucleus -- Physiopathology
  • Hearing Loss, Noise-Induced -- Physiopathology
  • Tinnitus -- Physiopathology
ispartof: Proceedings of the National Academy of Sciences of the United States of America, 22 May 2012, Vol.109(21), pp.8292-7
description: Exposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of hyperactivity, remain poorly explored. Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal...
language: eng
source:
identifier: E-ISSN: 1091-6490 ; PMID: 22566618 Version:1 ; DOI: 10.1073/pnas.1116981109
fulltext: fulltext
issn:
  • 10916490
  • 1091-6490
url: Link


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titleMechanisms contributing to central excitability changes during hearing loss
creatorPilati, Nadia ; Ison, Matias J ; Barker, Matthew ; Mulheran, Mike ; Large, Charles H ; Forsythe, Ian D ; Matthias, John ; Hamann, Martine
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subjectCochlear Nerve -- Physiopathology ; Cochlear Nucleus -- Physiopathology ; Hearing Loss, Noise-Induced -- Physiopathology ; Tinnitus -- Physiopathology
descriptionExposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of hyperactivity, remain poorly explored. Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal...
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titleMechanisms contributing to central excitability changes during hearing loss
descriptionExposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of hyperactivity, remain poorly explored. Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal...
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abstractExposure to loud sound causes cochlear damage resulting in hearing loss and tinnitus. Tinnitus has been related to hyperactivity in the central auditory pathway occurring weeks after loud sound exposure. However, central excitability changes concomitant to hearing loss and preceding those periods of hyperactivity, remain poorly explored. Here we investigate mechanisms contributing to excitability changes in the dorsal cochlear nucleus (DCN) shortly after exposure to loud sound that produces hearing loss. We show that acoustic overexposure alters synaptic transmission originating from the auditory and the multisensory pathway within the DCN in different ways. A reduction in the number of myelinated auditory nerve fibers leads to a reduced maximal firing rate of DCN principal cells, which cannot be restored by increasing auditory nerve fiber recruitment. In contrast, a decreased membrane resistance of DCN granule cells (multisensory inputs) leads to a reduced maximal firing rate of DCN principal...
doi10.1073/pnas.1116981109
pmid22566618
date2012-05-22