Dysfunction of Calcium Regulation Mediates Processes Involved in Age-Related Hearing Loss

Abstract

Hearing loss is a complicated disability affecting a substantial portion of the public. Hearing loss can occur due to a variety of reasons, but the processes involved in such a phenomenon are considered to be similar across all types of hearing loss. Here, an oncomodulin knock-out (KO) mouse strain is used to resemble an age-related hearing loss model. Oncomodulin (OCM) is a calcium binding protein (CaBP) in mammalian outer hair cells (OHC) responsible for calcium regulation. OCM is the dominant CaBP and is the only known CaBP whose KO is known to cause progressive hearing loss. Thus, this study sought to examine changes in the OHC that occur in response to its deletion. Of interest were OHC survivability, electromotive function, efferent cluster connections, and secondary CaBP expression, all of which are proposed mechanisms involved in hearing loss. This study hypothesized that the calcium dysfunction resulting from Ocm KO leads to changes in these four areas, which contributes to eventual hearing loss. Upon analysis, it was found that OHC survivability and efferent cluster expression are mediated by calcium regulation, while secondary CaBP activity and electromotive function appear unaffected. These findings suggest that OHC presence and efferent connections are primarily involved in processes resulting in age-related hearing loss, and that these mechanisms are regulated by OCM function.