He has granted you from all that you ask Him. Were you to attempt to count God's blessings, you could not compute them. But for sure, humankind is much prone to wrongdoing (sins and errors of judgment) and to ingratitude.

(Ibrahim 14:34)

Today a large part of modern science focuses on understanding the human body. Researchers working on life sciences hope that one day the secrets of every single detail that make us human will be revealed. Every year billions of dollars are spent by scientific institutions on learning more about us. Actually this fact by itself is enough to suggest how little control we have over things happening in our bodies, and we know even less about the mechanisms of moving, touching, speaking, seeing, or hearing, and so on.

As a scientist, I really cannot guess whether life scientists will ever be able to learn enough to solve the puzzles of the human body, but I feel a lack of satisfaction when the knowledge we have gained from scientific discoveries is compared with what is unknown. In my opinion this is why one of the most intelligent physicists in history, the Nobel laureate Richard Feynman, once said, “I was born not knowing, and have only had a little time to change that here and there” [1]. My understanding is that such a conclusion must be inevitable if the primitive knowledge given to us by modern sciences is not interpreted in the light of a far superior logic that is meant to explain the whole creation. In that sense, I believe that we have to consider every single detail in creation as a vital part of the whole in order not to feel lost before the grand picture of this masterpiece.

Last year, in a seminar at Osaka University Graduate School for Frontier BioSciences, I was thrilled to hear Professor Keichi Namba say, “Japan’s fastest supercomputer dissipates more than billion times the power dissipated by a fly’s brain, yet it is not able to simulate the brain of such a tiny animal.” This worked as a wakening call or a reminder for me to think again about the magnificent arts of the Creator. In particular, I wanted to revise my research on a hearing-related protein from a new perspective, rather than using the mechanical attitude that is followed most of the time.

This article is an attempt to explain an amazing mechanism in our ears that enables us to hear the faintest whispers. A mechanism that is switched off at loud cries to protect us from disturbing noises, yet amplified to make the softest sounds audible. Before starting to explain the basic anatomy of the human ear, I should mention that today the ear’s active amplification mechanism is still being investigated in research centers by biologists and physicists together.

How do we hear? What is happening in the inner ear?

Findings from the last century have shown that our ears are not just simple receivers as we had imagined. In 1979, David Kemp of University College, London discovered that mammalian ears can also emit sound vibrations. By placing a very sensitive microphone close to the eardrum he could detect whistles, implying that there is a source of vibration within the ear [2]. However, before trying to explain the cause of vibrations in the ears, we have to go over the mechanism of hearing briefly: The delicate design of the outer ear, the tympanic membrane (eardrum), and the tiny bones (malleus, incus and stapes) enables to collect sound waves traveling in the medium and transfer them to the inner ear (Figure 1a). In the inner ear the sound waves are sorted according to their frequency and amplitudes and then converted into electrical signals which can be transported to the brain via nerves. At the onset of this process the sound waves are transformed into standing waves on the basilar membrane which is laid along the organ resembling a snail, the cochlea (Figure 1b). The frequency of the incoming sound wave determines the positions of the distortions along the cochlea: High pitches create vibrations at the basal end of the cochlea (i.e. adjacent to the middle ear) whereas low frequencies vibrate closer to the apical end (Figure 1c) where the cochlea gets narrower. This geometry helps our ears to act as a frequency analyzer.

The efferent and afferent nerves that connect the ear to the central nervous system are attached to the organ of Corti, which is situated right next to the basilar membrane, extending over the cochlea. In other words, Corti is the sense organ of hearing, converting the motion of the basilar membrane into electrical signals that are conducted to the brain via neuronal cells [3]. The organ of Corti is also lined with multiple rows of sensory hair cells.

The hair cells of the organ of Corti

Corti is decorated with two different sets of sensory cells: single row of inner hair cells (IHCs) accompanied with 3–4 rows of outer hair cells (OHCs), both spanning the whole cochlear tube (Figure 2a). They are called “hair cells” because both IHCs and OHCs have typical bundles of stereocilia that contain mechanosensitive ion channels (Figure 2b).

The major function of IHCs is to detect the sound waves and then convert them into equivalent electrical signals that are to be interpreted by the brain. When the basilar membrane is perturbed by the incoming sound waves, the IHCs found in that region sense this activity by the movement of their hair bundles (bundles of stereocilia). The hair bundles of IHCs deflect and re-align as the basilar membrane moves up and down (Figure 3). We should note that this is an amazingly sensitive process such that deflections of the stereocilia on the order of a few nanometers (one millionth of a millimeter) can be detected and converted into nerve signals by the IHCs [4].

However, this by itself is not sufficient for hearing; no matter how effective IHCs work, the fluid that fills the cochlear tube is a threat to the sound waves traveling in the inner ear. In 1948, a young astrophysicist named Thomas Gold was the first person who has pointed out that the fluidic nature of the cochlea would dampen the sound vibrations and make them too weak to be detected by IHCs. He has concluded that an inherent vibration amplification mechanism is necessary in order to overcome such a problem [5]. Unfortunately, Gold’s statements were overlooked by the physiologists of his time who had performed their hearing related experiments on dead cochleas.

Gold’s predictions were justified around ten years later by William Rhode, a physiologist from University of Wisconsin, who has shown that the vibrations of the basilar membrane in live tissue samples are stronger than anticipated [6]. In the present day the existence of an amplification mechanism within a live cochlea is a well accepted fact. The only disagreement among scientists is about how the mechanism of the amplification works. Several scientific laboratories have reported different experiments performed on the organ of Corti and they have proposed different models. At the center of one of these models is prestin, a membrane protein which is not found in any cell but OHCs in the human body.

Electro-motile outer hair cells and prestin

In 1985, the distinctive properties of OHCs were first discovered by William Brownell, a University of Geneva neuroscientist, who has shown that these cells can convert electrical signals into motion: A phenomenon called electromotility. Electromotile OHCs can elongate or shrink in response to electrical charge density changes in their membranes. About a decade ago Peter Dallos and co-workers from Northwestern University in Chicago discovered a membrane protein, unique to OHCs, that can respond to electrical signals [3]. The Dallos group coined the name “prestin” for this protein in an analogy with the musical term “presto” (quickly) due to its rapid response to electrical signals. Various kinds of mammalian cells genetically engineered to produce prestin at their membranes displayed the electromotile responses that are very similar to OHCs.

According to Peter Dallos prestin protein works as a tiny machine which is a crucial element for cochlear amplification [7]. His theory is verified by recent studies which show that cochlear sensitivity in mice decreases hundredfold when prestin activity is disrupted by genetic means [8]. As the sound waves reach the inner ear, prestin-driven electromotility enables the OHCs to move like pistons. The piston movement in phase with the basilar membrane motion amplifies the vibrations and makes them stronger for IHC detection (Figure 4a,b). The prestin-driven vibrations were what Thomas Gold proposed and David Kemp had detected so many years ago. However, scientists are still searching and learning new things about this nanometer scale machine. One of the discoveries showed that prestin can adjust itself according to the amplitude of the incoming sound waves: Basically, the amplification is stronger when the sound waves are hard to hear but gets weaker as the volume increases.

Up to this point, we have briefly explained how the amplification mechanism of hearing in mammals works. Unfortunately, even though it took decades of research for scientists to discover and define the active nature of the mammalian ear, this explanation highlights only a minuscule part of the whole picture. That is why we are still incapable of curing most hearing problems. For example, hearing loss due to slightly disturbed hair cells with damaged stereocilia turns out to be chronic (Figure 5). The medical treatments we have to hand are too primitive to mend such delicate structures. Moreover, hearing aids made by today’s technology are not nearly as effective and functional as needed.

On the other hand, the delicacy of the hair cells and the limited control scientists have over them are not the only lessons we have learned from research on the inner ear. We cannot overlook the other messages attached to the research on the grounds that the time given to us is just too short to comprehend. It is an undeniable fact that the sense of hearing is designed in the best way to serve human beings. The different characteristics of hearing amplification at different sound levels make life much easier for us: Prestin-driven hearing is most effective when the sound waves are weak and harder to hear. This way the incoming sound waves are amplified enabling us to hear the faintest whispers. However, as the sound strength increases, the prestin-driven amplification gradually gets weaker and finally diminishes after a point to make sure that loud noises are less disturbing and hazardous for us. In my opinion, this amazing quality of a tiny protein found in our ears is one of the pieces of evidence that remind us of the necessity of pondering the favors of our Creator. Qur’anic verses such as Ibrahim 34 at the beginning of this article give us clues about how to interpret scientific findings that reveal the amazing qualities of our bodily organs. May the Creator of our ears allow us to reflect more on His favors and live accordingly.

Hamdi Sener is a biophysicist living in Boston. He can be contacted at This email address is being protected from spambots. You need JavaScript enabled to view it..


1. Gleick, J., Genius: The Life and Science of Richard Feynman. Reprint ed. 1993: Vintage. 560.

2. Kemp, D.T., The evoked cochlear mechanical response and the auditory microstructure- evidence for a new element in cochlear mechanics. Scand Audiol Suppl., 1979. 9: p. 35–47.

3. Zheng, J., et al., Prestin is the motor protein of cochlear outer hair cells. Nature, 2000. 405(6783): p. 149–55.

4. Robles, L. and M.A. Ruggero, Mechanics of the mammalian cochlea. Physiol Rev., 2001. 81(3): p. 1305–52.

5. Gold, T., Hearing II. The physical basis of the action of the cochlea. Proc. Roy. Soc. B., 1948. 135: p. 492–498.

6. Rhode, W.S., Observations of the vibration of the basilar membrane in squirrel monkeys using the Mossbauer technique. J. Acoust. Soc. Am. , 1971. 49: p. 1218–1231.

7. Cho, A., What's Shakin' in the ear? Science, 2000. 288: p. 1954-1955.

8. Liberman, M.C., et al., Prestin is required for electromotility of the outer hair cell and for the cochlear amplifier. Nature, 2003. 419: p. 300-304.

9. Fettiplace, R. and C.M. Hackney, The sensory and motor roles of auditory hair cells. Nat Rev Neurosci., 2006. 7(1): p. 19-29.

10. Dallos, P. and B. Fakler, Prestin, a new type of motor protein. Nat Rev Mol Cell Biol, 2002. 3(2): p. 104-11.

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