The significance of the calcium signal in the outer hair cells and its possible role in tinnitus of cochlear origin.

Finely tuned changes in intracellular Ca(2+) concentration modulate a variety of cellular functions in eukaryotic cells. The cytosolic Ca(2+) concentration is also tightly controlled in the outer hair cells (OHCs), the highly specialized receptor and effector cells in the mammalian auditory epithelium, which are responsible for high sensitivity and sharp frequency discrimination in hearing. OHCs possess a complex system of transporters, pumps, exchangers, channels and binding proteins to develop and to halt the regulatory Ca(2+) signal. The crucial role of elevated intracellular Ca(2+) concentration in OHCs is to increase the efficacy of the electromechanical (electromotile) feedback via remodeling of the cortical cytoskeleton. Anomalies in the Ca(2+) signaling pathway may lead to hypersensitivity of the cochlear amplifier and subsequently trigger tinnitus of cochlear origin. This review describes the dynamics of Ca(2+) signaling in the OHCs and a model that may convey a putative mechanism of development of subjective idiopathic cochlear tinnitus.