Abstract:
Sound transduction in the cochlea is accomplished by flow of K+ through sensory hair cells and essential to this process is the maintenance of the K+ concentration and positive endocochlear potential (EP) in the endolymph. Regulation of the endolymph electrochemical composition and volume is achieved by controlled secretion of K+ by the stria vascularis and its subsequent transport across the heterogenous epithelium surrounding the endolymphatic space. Ion extrusion is coordinated by a diverse group of K+ transport proteins and channels present in these cells. Disruption of these K+ transporters and channels may have adverse effects on endolymph and perilymph fluid regulation, contributing to auditory pathologies such as Ménière's syndrome, noise-induced hearing loss and potentially, in cochlear aging. Regulation of the electrochemical profile and how this changes in disease states is not well understood. As part of a larger study to investigate how the age-related disruption of cochlear communication pathways affects K+ buffering, leading to loss of hearing sensitivity, this study investigated the expression of key K+ transporters in cochlear tissues and looked at changes with age. Immunohistochemistry was used to characterise the expression of K-Cl transporters (KCC1,3 and 4), NKCl cotransporter (NKCC) and NaKATPase in the C57BL/6 mouse cochlea at 1,6 and 12mths of age. There was no expression of KCC1 at any age and expression of KCC3 was inconclusive because of antibody specificity problems. KCC4 was expressed in the supporting cells of the organ of Corti and did not change with age, despite the loss of sensory cells. NaKATPase and NKCC were expressed mainly in the fibrocytes and epithelial cells of the lateral wall tissues in a specific distribution pattern. These did not change with age, despite loss of fibrocytes in the lateral wall. These data imply that the K+ pathways remain intact with age, indicating that further studies are needed to determine how changes in K+ homeostasis may contribute to agerelated hearing loss.