Figure 2. Hair cell transduction and cochlear amplification. A: Diagram of hair bundle illustrating interciliary links that allow the bundle to remain cohesive. Tip links are formed by CDH23 at the upper end and PCDH15 at the lower end. Myosin molecules present near the upper tip link density adjust the tension applied to the transduction channel at the lower end of the tip links. Displacements toward the longest stereocilia result in gating of the transduction channel and are considered excitatory. B: Transduction currents are elicited by a 0.25-µm square step stimulus toward to tallest stereocilia. Such displacement results in fast increase in channel open probability. Over the subsequent 100 ms, the probability declines or adapts to a new steady-state level. The stimulus-response relationship (right) shifts in the direction of the applied stimulus. In the example of a positive stimulus, the curve shifts to the right (dashed line). Concomitantly to the channel opening, a decrease in bundle stiffness can be observed. The change in stiffness results from the opening of the channels. C: Two components for cochlear amplification. Current models suggest that cochear amplification may be driven by two mechanisms: active hair bundle movement and somatic motility. Active hair bundle movements may result from the interplay between adaptation and bundle relaxation. Channel opening results in bundle relaxation and a displacement of the bundle in the excitatory direction. At the same time, when calcium enters the cell via the transduction channel, fast adaptation occurs, which resets the position of the tip links and generates a negative movement of the bundle. If the bundle is moved further, transduction channels reopen. Around Popen = 0.5, the system can become unstable, oscillating back and forth between the two states. Cochlear amplification may also be driven by somatic motility in OHCs via activation of the prestin molecules densely packed along the basolateral membrane.