Spiral ganglion neurons (SGNs) within the cochlea degenerate following the loss of the auditory sensory epithelium, the auditory hair cells. Since these neurons are the target cells of the cochlear implant, which bypasses damaged or lost hair cells to stimulate the SGNs directly, enhanced SGN number and integrity may provide enhanced outcomes for cochlear implant patients. Improved contact between the cochlear implant electrode array and the auditory nerve fibres is also likely to enhance the benefits received by cochlear implant patients. Therefore, the identification of molecules with the capacity to support SGN survival and stimulate axonal growth has significant clinical implications. Based on their roles in the development and maintenance of the auditory system, some neurotrophic factors are expected to play an important role in enhancing the survival of auditory elements following deafening. This thesis investigates various molecules for their capacity to stimulate and guide the growth of SGN axons, and also investigates the survival-promoting effects of specific neurotrophic factors on SGN survival in clinically relevant animal models of deafness. Two neurotrophic factors were identified specifically to stimulate axonal growth from SGNs in an in vitro model of deafness.
Identifer | oai:union.ndltd.org:ADTP/245177 |
Date | January 2004 |
Creators | Gillespie, Lisa N. |
Source Sets | Australiasian Digital Theses Program |
Language | English |
Detected Language | English |
Rights | Terms and Conditions: Copyright in works deposited in the University of Melbourne Eprints Repository (UMER) is retained by the copyright owner. The work may not be altered without permission from the copyright owner. Readers may only, download, print, and save electronic copies of whole works for their own personal non-commercial use. Any use that exceeds these limits requires permission from the copyright owner. Attribution is essential when quoting or paraphrasing from these works., Open Access |
Page generated in 0.0015 seconds