Structural and Ultrastructural Changes to Type I Spiral Ganglion Neurons and Schwann Cells in the Deafened Guinea Pig Cochlea

dc.contributor.authorWise, Andrew
dc.contributor.authorPujol, Remy
dc.contributor.authorLandry, Thomas
dc.contributor.authorFallon, James
dc.contributor.authorShepherd, Robert
dc.date.accessioned2018-07-03T03:35:11Z
dc.date.available2018-07-03T03:35:11Z
dc.date.issued2017-07
dc.description.abstractSensorineural hearing loss is commonly caused by damage to cochlear sensory hair cells. Coinciding with hair cell degeneration, the peripheral fibres of type I spiral ganglion neurons (SGNs) that normally form synaptic connections with the inner hair cell gradually degenerate. We examined the time course of these degenerative changes in type I SGNs and their satellite Schwann cells at the ultrastructural level in guinea pigs at 2, 6, and 12 weeks following aminoglycoside-induced hearing loss. Degeneration of the peripheral fibres occurred prior to the degeneration of the type I SGN soma and was characterised by shrinkage of the fibre followed by retraction of the axoplasm, often leaving a normal myelin lumen devoid of axoplasmic content. A statistically significant reduction in the cross-sectional area of peripheral fibres was evident as early as 2 weeks following deafening (p < 0.001, ANOVA). This was followed by a decrease in type I SGN density within Rosenthal's canal that was statistically significant 6 weeks following deafening (p < 0.001, ANOVA). At any time point examined, few type I SGN soma were observed undergoing degeneration, implying that once initiated, soma degeneration was rapid. While there was a significant reduction in soma area as well as changes to the morphology of the soma, the ultrastructure of surviving type I SGN soma appeared relatively normal over the 12-week period following deafening. Satellite Schwann cells exhibited greater survival traits than their type I SGN; however, on loss of neural contact, they reverted to a non-myelinating phenotype, exhibiting an astrocyte-like morphology with the formation of processes that appeared to be searching for new neural targets. In 6- and 12-week deafened cochlea, we observed cellular interaction between Schwann cell processes and residual SGNs that distorted the morphology of the SGN soma. Understanding the response of SGNs, Schwann cells, and the complex relationship between them following aminoglycoside deafening is important if we are to develop effective therapeutic techniques designed to rescue SGNs.en_US
dc.description.sponsorshipThe authors would like to acknowledge the funding support from the NIDCD (HHS-N-263-2007-00053-c and R01DC015031) and the NHMRC (GNT1064375). The Bionics Institute acknowledges the support it receives from the Victorian Government through its Operational Infrastructure Support Program.en_US
dc.identifier.citationWise, A. K., R. Pujol, T. G. Landry, J. B. Fallon, and R. K. Shepherd. 2017. Structural and Ultrastructural Changes to Type I Spiral Ganglion Neurons and Schwann Cells in the Deafened Guinea Pig Cochlea. Journal of the Association for Research in Otolaryngology : JARO. 18(6): 751-769.en_US
dc.identifier.issn1438-7573
dc.identifier.urihttp://repository.bionicsinstitute.org:8080/handle/123456789/305
dc.language.isoenen_US
dc.publisherSpringerLinken_US
dc.subjectSpiral ganglion neuronen_US
dc.subjectSchwann cellen_US
dc.subjectDeafnessen_US
dc.subjectNerve degenerationen_US
dc.subjectNerve regenerationen_US
dc.subjectCochlear implanten_US
dc.titleStructural and Ultrastructural Changes to Type I Spiral Ganglion Neurons and Schwann Cells in the Deafened Guinea Pig Cochleaen_US
dc.typeArticleen_US
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