Electronic Thesis and Dissertation Repository

Degree

Doctor of Philosophy

Program

Neuroscience

Supervisor

Dr. Elizabeth Hampson

Abstract

Otoacoustic emissions (OAEs) are a naturally occurring by-product of the outer hair cells in the cochlea of the inner ear. A sexual dimorphism in OAE production favouring females has been reported in both human and non-human species. The broad objective of the present set of studies is to explore how the sexual dimorphism originates and the degree to which it reflects the organizational and activational influences of sex steroid hormones.

Most previous studies of sex differences in OAEs have been based on neonatal, infant, or broad adult samples, Study 1 of the present work was done to verify the reported sex difference, both in spontaneously produced OAEs (spontaneous OAEs or SOAEs) and in OAEs produced in response to acoustic stimuli (click-evoked OAEs or CEOAEs), in a sample of non-hearing impaired young adults. Ear differences in OAE production also have been reported, and this study investigated whether hand preference moderates the observed ear asymmetry in OAE production. Although a robust sex difference was documented in the numbers and powers of SOAEs produced, and in CEOAE response amplitude, there was no evidence to support a reduced ear asymmetry in left-handers.

The major theory purporting to explain the sex difference in OAE production proposes that prenatal androgen exposure in the male fetus dampens the cochlear mechanisms responsible for OAE production and is responsible for the observed sex difference in this trait. In order to test the proposed organizational influence on OAE production, the relationship between OAEs and the ratio of the lengths of the 2nd to 4th digits (the 2D:4D ratio), a marker of individual variations in prenatal androgen exposure, was examined in Study 2. A significant correlation between OAE production and 2D:4D digit-ratios was not found. Fundamental differences in the prenatal development of these characteristics, however, may explain the lack of correlation and do not preclude a prenatal hormonal influence on OAE production.

Another source of variation that may contribute to the sex difference in OAE production is circulating levels of adult steroids. Evidence supporting this possibility is limited. Studies 3 and 4 provided a novel test of the hypothesized activational influence of sex steroids in women and men. Oral contraceptive use in women, which reliably decreases circulating sex steroids, was shown to be associated with reduced OAE production compared to normally-cycling women (Study 3). In Study 4, a negative correlation was found between CEOAE response amplitude and circulating testosterone levels in men. Thus, it appears in men that elevations in circulating testosterone diminish OAE production in a manner similar to that hypothesized prenatally, whereas the results in women suggest that estradiol may influence OAE production in adulthood. These are the first systematic studies to support an activational effect of circulating steroids on OAE production in humans.


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