Uniquely among sensory receptors the hair cell is not a passive recipient of stimuli, but instead uses an active process to enhance its inputs. The active process amplifies mechanical stimuli by as much as a thousandfold, thus greatly increasing our sensitivity to weak sounds. When this process fails, we become hard of hearing. Amplification is accompanied by frequency tuning, which restricts each hair cell's response to a narrow frequency band. If the active process deteriorates, we grow less sensitive to subtle differences in frequency and therefore suffer a diminished ability to discriminate sound sources. Finally, the active process produces a compressive nonlinearity that renders the ear sensitive to sounds over an astonishing trillionfold range in power. By enhancing weak stimuli and suppressing strong ones, this feature allows us to enjoy an instrumental soloist as comfortably as a full orchestra one hundred times as loud.
Two mechanisms cooperate in the active process of the mammalian cochlea. First, hair bundles serve not only as transducers but also as amplifiers. For sounds of relatively low frequency, myosin-1c motors attached at the upper insertions of tip links provide the motive force that enhances hair-bundle motion in response to weak stimuli. The other motile phenomenon involves changes in the length of a hair cell's entire soma. The plasmalemma of each outer hair cell is studded with millions of copies of the protein prestin. Changes in voltage alter the membrane area occupied by these molecules: depolarization causes a hair cell to shorten whereas hyperpolarization provokes elongation. These periodic changes in length pump energy into the basilar membrane's oscillation. The three cardinal features of the active process-amplification, frequency tuning, and compressive nonlinearity-emerge together because this dynamical system operates near an instability called the Hopf bifurcation.
