Ion channel protein interactions in the mammalian ear

Abstract

Problem: Electrical activity in hair cells and neurons of the inner ear is necessary for the transduction and modulation of stimuli impinging on the cochlea and vestibular endorgans of the inner ear. The underlying bases of this activity are pore-forming proteins in the membrane of excitable cells that allow the influx and efflux of various ions including Na+, Ca2+, and K+, among others. These channels are critical to both electrical activity and the development of excitable cells since they may initiate long-term signals important in the maintenance and survival of these cells. We investigate the expression of Shaker and Shal potassium ion channel proteins in the vestibular endorgans of mammalian species including mouse and human. Methods: Vestibular tissue was harvested from adult mice as well as human subjects undergoing vestibular surgery. Western blot analysis was used to identify the presence or absence of alpha subunits Kv1.2, Kv1.4, Kv1.5, Kv4.2, and beta subunit Kvâ1.1 in mouse. Immunohistochemistry was then used to localize Kv1.2 in mouse and human tissue. Results: The presence of alpha subunit Kv1.2 and beta subunit Kvâ1.1 was confirmed in adult mouse vestibular tissue by Western blotting. Immunostaining was used to localize potassium ion channel Kv1.2 to the vestibular endorgans of mouse and human. In comparison neither Kv 1.4, Kv1.5, nor Kv4.2 was found in the vestibular tissue. Conclusion: We describe the presence and location of various potassium ion channel alpha and beta subunits. These data are initial descriptions of potassium ion channels in the mammalian vestibular system and begin to provide an understanding of the protein subunits that form ion channels of the mammalian inner ear. This knowledge is critical to understanding the genetics of these channels and finding cures for pathologies of hearing and balance. Significance: We detail initial characteristics of potassium ion channel proteins including alpha subunit Kv1.2, Kv1.4, Kv1.5, Kv4.2, and beta subunit Kvâ1.1 in mammalian vestibular tissue. This knowledge is critical as mutations can cause neurological pathologies including auditory and vestibular disorders. Support: AAO-HNSF Resident Research Grant 2002