Estradiol (E) is a multitasking hormone that plays a prominent role in the reproductive system, and also contributes to physiological and growth mechanisms throughout the body. Frisina and colleagues have previously demonstrated the beneficial effects of this hormone, with E‐treated subjects maintaining low auditory brainstem response (ABR) thresholds relative to control subjects (Proceedings of the National Academy of Sciences of the United States of America, 2006;103:14246; Hearing Research, 2009;252:29). In the present study, we evaluated the functionality of the peripheral and central auditory systems in female CBA/CaJ middle‐aged mice during and after long‐term hormone replacement therapy (HRT) via electrophysiological and molecular techniques. Surprisingly, there are very few investigations about the side effects of HRT in the auditory system after it has been discontinued. Our results show that the long‐term effects of HRT are permanent on ABR thresholds and ABR gap‐in‐noise (GIN) amplitude levels. E‐treated animals had lower thresholds and higher amplitude values compared to other hormone treatment subject groups. Interestingly, progesterone (P)‐treated animals had ABR thresholds that increased but amplitude levels that remained relatively the same throughout treatment. These results were consistent with qPCR experiments that displayed high levels of IGF‐1R in the stria vascularis (SV) of both E and P animal groups compared to combination treatment (E + P) animals. IGF‐1R plays a vital role in mediating anti‐apoptotic responses via the PI3K/AKT pathway. Overall, our findings gain insights into the neuro‐protective properties of E hormone treatments as well as expand the scientific knowledge base to help women decide whether HRT is the right choice for them.

The CBA/CaJ mouse strain's auditory function is normal during the early phases of life and gradually declines over its lifespan, much like human age-related hearing loss (ARHL), but on a mouse life cycle “time frame”. This pattern of ARHL is relatively similar to that of most humans: difficult to clinically diagnose at its onset, and currently not treatable medically. To address the challenge of early diagnosis, CBA mice were used for the present study to analyze the beginning stages and functional onset biomarkers of ARHL. The results from Auditory Brainstem Response (ABR) audiogram and Gap-in-noise (GIN) ABR tests were compared for two groups of mice of different ages, young adult and middle age. ABR peak components from the middle age group displayed minor changes in audibility, but had a significantly higher prolonged peak latency and decreased peak amplitude in response to temporal gaps in comparison to the young adult group. The results for the younger subjects revealed gap thresholds and recovery rates that were comparable to previous studies of auditory neural gap coding. Our findings suggest that age-linked degeneration of the peripheral and brainstem auditory system is already beginning in middle age, allowing for the possibility of preventative biomedical or hearing protection measures to be implemented as a possibility for attenuating further damage to the auditory system due to ARHL.

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Hormones such as estrogen, progesterone, and aldosterone all demonstrate vital roles in sustaining auditory function through either the maintenance of cochlear neurons, up/down regulation of critical molecules (i.e., IGF‐1, BDNF, etc.), or generation of the endocochlear potential. With disease and/or age, hormone expression begins to decline drastically, which ultimately affects cochlear structures and the integrity of cochlear cells. The following review explores the latest findings as well as realistic outcomes for hormone therapy treatment in the auditory system. This information could serve as a potential guide for patients considering hormone therapy as a medicinal choice to alleviate the signs of onset of presbycusis—age‐related hearing loss. Additional scientific investigations could also be carried out to further enhance recent findings.

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