Preferred Name

Melissa Teller

Date of Award

Spring 2017

Document Type

Dissertation

Degree Name

Doctor of Audiology (AuD)

Department

Department of Communication Sciences and Disorders

Advisor(s)

Lincoln C. Gray

Christopher G. Clinard

Mark Gabriele

Abstract

It is known that EphA4 can influence the establishment of tonotopic pathways in the auditory system. This can be measured by an increase in thresholds on the auditory brainstem response test (ABR) in mice. It is also known that the aging population in humans tends to have poorer thresholds in the high frequency sounds as they age, termed presbycusis or age-related hearing loss. The C57BL/6J background strain of mice that is known to experience a presbycusis-like process, although it is not specified when this process begins and how it progresses through their life span. The goal of this study was to determine how the EphA4 mutation on a C57BL/6J background strain can affect the hearing of mice at different ages. ABR measures were recorded in mice between 2-9 months of age with and without the EphA4 lacZ mutation. Analysis of ABR threshold showed similar results to previous studies for mice with the homozygous mutation (EphA4lacZ/lacZ). These mice have a rapid decrease in hearing starting early in life; our mice exhibited severe hearing loss even as young as 2 months of age. When we analyzed threshold data for the heterozygous and wild type mice, we found that mice with the heterozygous mutation (EphA4lacZ/+) had some preservation of their hearing thresholds using a mid-frequency stimulus (8kHz tone pip) when compared to their wild type littermates (EphA4+/+). When using a high-frequency stimulus (12kHz tone pip), both groups had equally poor thresholds. This suggests a heterozygote advantage which preserves their mid-frequency hearing longer and slows down the process of presbycusis. This may have implications for potentially delaying the process of human presbycusis and preserving hearing into later ages.

Available for download on Friday, April 19, 2019

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