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Computational modeling of the effects of auditory nerve dysmyelination.

Brown AM, Hamann M - Front Neuroanat (2014)

Bottom Line: 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).

View Article: PubMed Central - PubMed

Affiliation: School of Biomedical Sciences, Queens Medical Centre, University of Nottingham Nottingham, UK.

ABSTRACT
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).

No MeSH data available.


Related in: MedlinePlus

Action potential conduction along the central portion of the auditory nerve. (A) Schematic model of the axonal compartments in the control auditory nerve model. (B) Evoked action potentials recorded at six successive nodes illustrating action potential conduction along an axon. Scale bar is 50 mV and the duration of the recording is 2 ms. (C) The conduction velocity decreases as internodal length (INL) is increased from the control value of 100 μm.
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Figure 2: Action potential conduction along the central portion of the auditory nerve. (A) Schematic model of the axonal compartments in the control auditory nerve model. (B) Evoked action potentials recorded at six successive nodes illustrating action potential conduction along an axon. Scale bar is 50 mV and the duration of the recording is 2 ms. (C) The conduction velocity decreases as internodal length (INL) is increased from the control value of 100 μm.

Mentions: The morphological dimensions of the axonal compartments have recently been published (Tagoe et al., 2014). The model of the control axon comprised alternating nodal and internodal regions (INR). The INRs were subdivided into paranodal (PN), juxtaparanodal (JP) and axonal compartments (Figure 2A), such that each INR comprised two PNs, each abutting consecutive nodal regions, two JP regions located between the PN and a central axonal portion (Figure 2A). The dimensions of the compartments are contained in Table 1. AOE changed the nodal length and diameter from 1.3 to 6.15 μm and 0.8 to 1.28 μm, respectively; the PN length and diameter from 2.34 to 1.52 μm and 0.75 to 1.23 μm respectively and the JP length and diameter from 5.14 to 6.23 μm and 2.13 to 1.32 μm respectively (Tagoe et al., 2014). The model contained a fast sodium current (INa), a high threshold (IHT) Kv3.1 potassium current, a low threshold (ILT) Kv1.1 potassium current and a leak current (IL). We assumed that the current density for INa and IHT in the nodal region were 6.6 mS.cm−2 and 1.98 mS.cm−2, respectively, and the value for ILT in the PN was 2.13 mS.cm−2 (Kanemasa et al., 1995).


Computational modeling of the effects of auditory nerve dysmyelination.

Brown AM, Hamann M - Front Neuroanat (2014)

Action potential conduction along the central portion of the auditory nerve. (A) Schematic model of the axonal compartments in the control auditory nerve model. (B) Evoked action potentials recorded at six successive nodes illustrating action potential conduction along an axon. Scale bar is 50 mV and the duration of the recording is 2 ms. (C) The conduction velocity decreases as internodal length (INL) is increased from the control value of 100 μm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4117982&req=5

Figure 2: Action potential conduction along the central portion of the auditory nerve. (A) Schematic model of the axonal compartments in the control auditory nerve model. (B) Evoked action potentials recorded at six successive nodes illustrating action potential conduction along an axon. Scale bar is 50 mV and the duration of the recording is 2 ms. (C) The conduction velocity decreases as internodal length (INL) is increased from the control value of 100 μm.
Mentions: The morphological dimensions of the axonal compartments have recently been published (Tagoe et al., 2014). The model of the control axon comprised alternating nodal and internodal regions (INR). The INRs were subdivided into paranodal (PN), juxtaparanodal (JP) and axonal compartments (Figure 2A), such that each INR comprised two PNs, each abutting consecutive nodal regions, two JP regions located between the PN and a central axonal portion (Figure 2A). The dimensions of the compartments are contained in Table 1. AOE changed the nodal length and diameter from 1.3 to 6.15 μm and 0.8 to 1.28 μm, respectively; the PN length and diameter from 2.34 to 1.52 μm and 0.75 to 1.23 μm respectively and the JP length and diameter from 5.14 to 6.23 μm and 2.13 to 1.32 μm respectively (Tagoe et al., 2014). The model contained a fast sodium current (INa), a high threshold (IHT) Kv3.1 potassium current, a low threshold (ILT) Kv1.1 potassium current and a leak current (IL). We assumed that the current density for INa and IHT in the nodal region were 6.6 mS.cm−2 and 1.98 mS.cm−2, respectively, and the value for ILT in the PN was 2.13 mS.cm−2 (Kanemasa et al., 1995).

Bottom Line: 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).

View Article: PubMed Central - PubMed

Affiliation: School of Biomedical Sciences, Queens Medical Centre, University of Nottingham Nottingham, UK.

ABSTRACT
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).

No MeSH data available.


Related in: MedlinePlus