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


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Article Info

DATE

2017-07-17

AUTHORS

Andrew K. Wise, Remy Pujol, Thomas G. Landry, James B. Fallon, Robert K. Shepherd

ABSTRACT

Sensorineural 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. More... »

PAGES

751-769

References to SciGraph publications

  • 2003-01-15. Changes in Cytochemistry of Sensory and Nonsensory Cells in Gentamicin-Treated Cochleas in JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY
  • 2014-05-01. Inhibition of the Activation and Recruitment of Microglia-Like Cells Protects Against Neomycin-Induced Ototoxicity in MOLECULAR NEUROBIOLOGY
  • 2013-11-12. Advances in peripheral nerve regeneration in NATURE REVIEWS NEUROLOGY
  • 1973-03. Ultrastructural features of neurons and nerve fibres in the spiral ganglia of cats in BRAIN CELL BIOLOGY
  • 2014-01-30. Examining the Electro-Neural Interface of Cochlear Implant Users Using Psychophysics, CT Scans, and Speech Understanding in JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY
  • 1999-10. Morphological and molecular changes in the inner hair cell region of the rat cochlea after amikacin treatment in BRAIN CELL BIOLOGY
  • 2009-11-21. Expression of Fractalkine Receptor CX3CR1 on Cochlear Macrophages Influences Survival of Hair Cells Following Ototoxic Injury in JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY
  • 2003-01-15. Distribution of Gentamicin in the Guinea Pig Inner Ear after Local or Systemic Application in JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY
  • 1997-08. Loss And Survival of Spiral Ganglion Neurons in the Guinea Pig After Intracochlear Perfusion with Aminoglycosides in BRAIN CELL BIOLOGY
  • 2013-02-08. Effects of Brain-Derived Neurotrophic Factor (BDNF) and Electrical Stimulation on Survival and Function of Cochlear Spiral Ganglion Neurons in Deafened, Developing Cats in JOURNAL OF THE ASSOCIATION FOR RESEARCH IN OTOLARYNGOLOGY
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    http://scigraph.springernature.com/pub.10.1007/s10162-017-0631-y

    DOI

    http://dx.doi.org/10.1007/s10162-017-0631-y

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1090745261

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/28717876


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