How hearing happens in the inner ear.
Why are mammals so soft and unprotected, ourselves most of all, being naked? One answer, evolutionarily, is that we are high instrumented, with exquisite senses of vision, touch, smell, position, and hearing, which project our defenses outward, from a hard exoskeleton to an over-the-horizon system, to put it in modern military parlance. Mammals have, for example, far better hearing than reptiles or other preceeding animals, both in frequency range and sensitivity. What is a lawnmower to us would be softly audible to a lizard, while what is pianissimo to us would not be audible at all. This was one of the super-powers that kept small insectivorous mammals going through the age of dinosaurs, both on the hunt and on defense against the velociraptors. High frequency hearing has been taken to particular extremes by cetaceans and bats.
A recent paper described the atomic structure of prestin, the key protein of the power-amplifier of mammalian hearing. But to understand its role, one needs some appreciation of the ornate engineering of our hearing apparatus, particularly the cochlea. The cochlea is the small snail-shaped organ that sits inside the hardest bone of our bodies. It is tonotopic, meaning that sound pitch is interpreted in order along its coiled length, as though it were an inverse piano keyboard. The highest frequency sounds are picked up at the beginning, near the oval window where the stapes connects with the cochlea, while lower-pitch sounds are detected at the tiny apex.
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| Schematic of the outer, middle, and inner ear. Note the direction of sound flow, first through the scala vestibuli of the cochlea, then around the apex, back through through the scala tympani, and to the pressure reliever of the round window. The basilar membrane sits in the middle, allowing excitation of itself when the frequency of the sound matches its intrinsic stiffness, which varies continuously along its length. |
Sound comes in via the eardrum and the small bones of the middle ear. Waves then propagate from the oval window through the fluid passages of the cochlea, (scala vestibuli), around the apex, and back out through the scala tympani to the round window, which is the final pressure reliever. Sound receptors are arranged along the central organ of Corti, (green), where the various frequencies are separately mapped and detected by the inner hair cells.
A Nobel prize was awarded in 1961 for the first viable explanation of how the cochlea works. At the core of the organ of Corti is the basilar membrane, whose width and stiffness varies continuously as its ribbon furls through the cochlea.
"When flattened and straightened, the basilar membrane appears wedge shaped, with its width gradually increasing from the cochlea’s “input” end (its base) toward the far end (its apex). The change in width results in a 1e4-to 1e5-fold reduction in the membrane’s stiffness from base to apex. This stiffness is conferred by the membrane’s dense strands of collagen fibers running perpendicular to the long dimension and making the membrane highly anisotropic"
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| An exaggerated standing wave excites its frequency-dependent point along the basilar membrane of the cochlea, here notionally stretched out for illustration. Lower frequencies are detected farther from the base. |
It is this stiffness that acts as a frequency selector, with each frequency exciting a standing wave at its own characteristic point along this basilar membrane, and thus along the length of the cochlea. The standing wave is detected by inner hair cells, which convert motion to electrical signals that go to the brain for processing and perception.
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| Cross-section of the basilar membrane, scala media, and associated cells, including especially the inner hair cells (IHC) which perceive sound and conduct resulting electrical signals to the brain, and the outer hair cells (O), which perceive sounds and set up a sympathetic positive feedback vibration, amplifying soft sounds thousands-fold, to assist the function of the inner hair cells. |
So far so good. But the cochlea also harbors outer hair cells, which are specific to mammals, and amplify our hearing by roughly 50 decibels. Yet these hair cells have far fewer nerve connections to the brain, and those connections do not map to the same auditory decoding areas as those from the inner hair cells. What gives? Well, it took till the 1970s to realize that the cochlea is not a passive organ, it is an active organ, one interesting sign of which are cochlear emissions. These are sounds coming out of the cochlea as a sort of amplified echo based on incoming lower amplitude sounds. It turns out that outer hair cells (which outnumber the inner hair cells on the basilar membrane) are not sensing nerve cells in the usual sense. Rather, they sense incoming sound and rapidly compress / decompress themselves, thus amplifying the signal vibration for the benefit of the inner hair cells, which then can relay a signal at far higher sensitivity than they could unassisted. This behavior is called electromotility.
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| Scanning electron micrograph (left) of outer hair cells with their cili at the top. DC are helper cells. At right is a dissected outer hair cells, with the stereocilia at top, cuticular plate, and nucleus at bottom. |
And how to outer hair cells perform this feat? Aside from a complex set of cilia at their tops, connecting to each other and to the tectorial membrane, plus alot of other intricate ionic physiology, they are covered (75% of their membranes along one side) with the protein prestin, which functions as a piezioelectric transducer. This protein is evolutionarily derived from a large family of anion transporters, so has 14 helical transmembrane protein segments that anchor it in the membrane, and has a sort-of-pore, which binds to anions like sulfate, chloride, and an inhibitor, salicylate. But this pore does not conduct any ions through the membrane. Instead, the change of local membrane voltage, which is induced by the firing of ion channels in the tips of the cilia, causes only a shape change, calculated via this new structure, of ~740 square angstroms reduction when electrically excited, which is about 10% of its total area. This is why the outer hair cell can contract extremely rapidly in reponse to the incoming frequency-discriminated sound signal. The energy for all this does not come (immediately) from ATP, as would be typical (but far to slow). No, it comes from an ionic environment that is specially tuned within the organ of Corti vs the neighboring fluid-fillled sound conduction channels (the scala vestibuli and the scala tympani directly underneath the basilar membrane), which create a potassium and charge gradient that allow the outer hair cells to fire without draining their own energy reserves.
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| Structures of prestin in activated (left) and relaxed (right) conformations. The overall area change of the protein induced by membrane charge changes leads to the contraction of the entire outer hair cell, in synchrony with the sound being perceived. |
Our hearing system is magnificent. One would tempted to call it a miracle of senstivity and discrimination, except that its long and painful evolution is clear, and its current incarnation remains subject to various deficiencies, like the various maladies of loss of hearing in old age, or the gain of tinnitus.
"The efficiency of conversion from mechanical force to electrical charge is estimated to be ~20 fC nN−1, four orders of magnitude greater than the efficiency of the best man-made piezoelectric material"
"The action of prestin is also orders of magnitude faster than that of any other cellular motor proteins."
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