Spiral ganglion neuron survival and function in the deafened cochlea following chronic neurotrophic treatment

dc.contributor.authorLandry, Thomas
dc.contributor.authorWise, Andrew
dc.contributor.authorFallon, James
dc.contributor.authorRobert, Shepherd
dc.date.accessioned2014-03-31T23:40:45Z
dc.date.available2014-03-31T23:40:45Z
dc.date.issued2011-12
dc.description.abstractCochlear implants electrically stimulate residual spiral ganglion neurons (SGNs) to provide auditory cues for the severe-profoundly deaf. However, SGNs gradually degenerate following cochlear hair cell loss, leaving fewer neurons available for stimulation. Providing an exogenous supply of neurotrophins (NTs) has been shown to prevent SGN degeneration, and when combined with chronic intracochlear electrical stimulation (ES) following a short period of deafness (5 days), may also promote the formation of new neurons. The present study assessed the histopathological response of guinea pig cochleae treated with NTs (brain-derived neurotrophic factor and neurotrophin-3) with and without ES over a four week period, initiated two weeks after deafening. Results were compared to both NT alone and artificial perilymph (AP) treated animals. AP/ES treated animals exhibited no evidence of SGN rescue compared with untreated deafened controls. In contrast, NT administration showed a significant SGN rescue effect in the lower and middle cochlear turns (two-way ANOVA, p < 0.05) compared with AP-treated control animals. ES in combination with NT did not enhance SGN survival compared with NT alone. SGN function was assessed by measuring electrically-evoked auditory brainstem response (EABR) thresholds. EABR thresholds following NT treatment were significantly lower than animals treated with AP (two-way ANOVA, p ¼ 0.033). Finally, the potential for induced neurogenesis following the combined treatment was investigated using a marker of DNA synthesis. However, no evidence of neurogenesis was observed in the SGN population. The results indicate that chronic NT delivery to the cochlea may be beneficial to cochlear implant patients by increasing the number of viable SGNs and decreasing activation thresholds compared to chronic ES alone.en_US
dc.description.sponsorshipThis study was funded by the National Institute on Deafness and Other Communication disorders (National Institutes of Health contract HHS-N-263-2007-00053-C), The Bartholomew Reardon PhD Scholarship (The Bionics Institute), and The Mabel Kent Scholarship. The Bionics Institute acknowledges the support it receives from the Victorian Government through its Operational Infrastructure Support Program.en_US
dc.identifier.citationLandry, T. G., Wise, A. K., Fallon, J. B., & Shepherd, R. K. (2011). Spiral ganglion neuron survival and function in the deafened cochlea following chronic neurotrophic treatment. Hearing Research, 282(1-2), 303-313. doi: 10.1016/j.heares.2011.06.007en_US
dc.identifier.urihttp://repository.bionicsinstitute.org:8080/handle/123456789/69
dc.language.isoenen_US
dc.publisherElsevieren_US
dc.subjectSGNen_US
dc.subjectNeurotrophinen_US
dc.subjectNeural Survivalen_US
dc.subjectDeafnessen_US
dc.subjectAuditory Systemen_US
dc.titleSpiral ganglion neuron survival and function in the deafened cochlea following chronic neurotrophic treatmenten_US
dc.typeArticleen_US
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