Auditory hair cells are specialized epithelial cells that are able to detect sound vibrations and convert them into electrical signals. The mammalian cochlear contains two classes of sensory hair cells that have distinct functions. Inner hair cells are responsible for detecting and encoding sound stimuli. Outer hair cells are thought to boost quiet stimuli by an electromechanical feedback process termed the ‘cochlear amplifier’ that increases sensitivity and frequency selectivity of our hearing. Mechanical vibrations are detected by the hair bundle that sits at the hair cell apex. In outer hair cells, mechanical displacement of the hair bundle with stiff glass fibers elicits a fast activating transducer current. The activation rate of the channel is too fast for us to measure; even at room temperature. In the presence of a maintained deflection the transducer current adapts with a very rapid time course, in the order of 100 µs (Kennedy et al., 2003). This rate of adaptation and the size of the transducer currents are dependent on the characteristic frequency of the cells, with high frequency cells showing much larger and faster adapting currents than low frequency cells (Ricci et al., 2005). In contrast, inner hair cells show slower adaptation time constants and the size and adaptation rate of the currents are not frequency dependent, but are uniform along the length of the cochlear (Beurg et al., 2006). These differences may reflect the different functions that inner and outer hair cells serve. Outer hair cells are thought to underlie the cochlear amplifier, and until recently, the only mechanism proposed in mammalian systems was mechanical force generation through cell length changes. This somatic motility is thought to be driven by receptor potential changes that drive conformational changes in the membrane protein Prestin. However, questions still remain about how Prestin would be driven at high frequencies when receptor potentials would be expected to be attenuated by the membrane time constant. In non mammalian systems amplification is achieved by the hair bundle. Force is thought to be generated by the mechano-transducer channel itself, which, unlike somatic motility, would not be limited by the membrane time constant of the cell. Experiments using flexible glass fibers have shown that outer hair cell bundles in mammalian hair cells are also capable of force generation, and that the rate of this force generation closely matches fast adaptation rates (Kennedy et al., 2005). As the rate of adaptation varies with characteristic frequency, so could force generation. In addition, as in non mammalian systems this mechanism would not be limited by the membrane time constant, making it an attractive candidate for the cochlear amplifier. However, questions still remain as to whether and how somatic motility or hair bundle force generation might underlie cochlear amplification. This presentation will summarize recent advances in our understanding of mechano-transduction in mammalian hair cells.