Abstract
To summarize advances in the study of the interaction between sensory hair cells and aminoglycoside antibiotics. Aminoglycosides enter hair cells through mechanotransduction channels and initiate an active signaling pathway that leads to cell death. Early expression of heat shock proteins can protect hair cells from aminoglycosides, although signaling from surrounding supporting cells appears to promote hair cell death. Studies of certain human deafness mutations have revealed new insights into the role of mitochondria in aminoglycoside ototoxicity. The cellular mechanisms of aminoglycoside ototoxicity continue to be an active topic of research and newly developed animal models offer great promise for future advances. Nevertheless, proven clinical methods for the prevention of ototoxic injury are not yet available.