Osmoreceptors in Cochlear Outer Hair Cells

Abstract

The mammalian outer hair cells (OHCs) are mechanical effectors of the cochlea. The slow motility of OHCs is considered to be a possible adaptive mechanism in the cochlea. It is suggested that passive calcium-independent slow motility induced by hyposmotic activation may have physiological or pathological significance even in normal or impaired hearing of cochlear origin. The cell swelling induced by hyposmotic stimulation has been shown to be accompanied by an increase of intracellular Ca2+ concentrations ([Ca2+]i) in OHCs. This [Ca2+]i increase may subsequently activate metabolic processes including phosphorylation in OHCs. Therefore, the ionic environment and the changes in osmolarity of the inner ear may affect the OHC motility, thereby varying the sensitivity of the inner ear to the sound. The functional expression of transient receptor potential vanilloid 4 (TRPV4) is involved in the hypotonic stimulation-induced Ca2+ influx in OHCs. It is suggested that TRPV4 may function as an osmo- and mechanosensory receptor in OHCs. Recent study showed that hyposmotic stimulation can induce nitric oxide (NO) production by the [Ca2+]i increase, which is presumably mediated by the activation of TRPV4 in OHCs. NO conversely inhibits the Ca2+ response via the NO-cGMP-PKG pathway by a feedback mechanism. Any disturbance in the homeostasis of inner ear fluids may therefore affect the functional properties of OHCs by NO via the activation of TRPV4, thereby influencing the delivery of auditory information. In this review, volume regulation in OHCs also will be discussed.