This article is part of the Research Topic Mathematical description of brain plasticity

Hypothesis & Theory ARTICLE

Front. Neuroanat., 01 August 2014 | doi: 10.3389/fnana.2014.00073

Computational modeling of the effects of auditory nerve dysmyelination

  • 1School of Biomedical Sciences, Queens Medical Centre, University of Nottingham, Nottingham, UK
  • 2Department of Cell Physiology and Pharmacology, University of Leicester, Leicester, UK

Our previous study showed that exposure to loud sound leading to hearing loss elongated the auditory nerve (AN) nodes of Ranvier and triggered notable morphological changes at paranodes and juxtaparanodes. Here we used computational modeling to examine how theoretical redistribution of voltage gated Na+, Kv3.1, and Kv1.1 channels along the AN may be responsible for the alterations of conduction property following acoustic over-exposure. Our modeling study infers that changes related to Na+ channel density (rather than the redistribution of voltage gated Na+, Kv3.1, and Kv1.1 channels) is the likely cause of the decreased conduction velocity and the conduction block observed after acoustic overexposure (AOE).

Keywords: myelin sheath, hearing loss, node of Ranvier, conduction velocity, conduction block, deafness, myelin domains, action potential

Citation: Brown AM and Hamann M (2014) Computational modeling of the effects of auditory nerve dysmyelination. Front. Neuroanat. 8:73. doi: 10.3389/fnana.2014.00073

Received: 18 March 2014; Paper pending published: 26 May 2014;
Accepted: 12 July 2014; Published online: 01 August 2014.

Edited by:

Anderson Mon, University of California San Francisco, USA

Reviewed by:

James C. Vickers, University of Tasmania, Australia
Ping Liu, University of Connecticut Health Center, USA

Copyright © 2014 Brown and Hamann. 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) or licensor 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.

*Correspondence: Martine Hamann, Department of Cell Physiology and Pharmacology, University of Leicester, Medical Sciences Building, PO Box 138, University Road, Leicester LE1 9HN, UK e-mail: mh86@le.ac.uk

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