In an effort to attempt to answer once and for all the hotly debated question of whether we can be stimulated by frequencies higher than the commonly accepted 20kHz - motivated by the HDCD patent's claim that there are nerve receptors up to about 80kHz - I have started reading medical research papers on the ear... This is probably just the beginning of a series of findings that I think I will be able to dig up, and is provided as food for thought, not definitive proof...
First of all, a little primer from Wikipedia:
From the Abstract:
The paper appropriately asks:
First of all, a little primer from Wikipedia:
In my initial research on OHCs - the amplifiers - I ran into this article http://physrev.physiology.org/content/88/1/173.full on Outer Hair Cell motility, which claims OHC length variations - thus stimulation - up to 79kHz, although the acceptable human hearing threshold is still defined at ~20kHz:Research of the past decades has shown that outer hair cells [OHCs] do not send neural signals to the brain, but that they mechanically amplify low-level sound that enters the cochlea. The amplification may be powered by movement of their hair bundles, or by an electrically driven motility of their cell bodies...
In mammalian outer hair cells, the receptor potential triggers active vibrations of the cell body. This mechanical response to electrical signals is termed somatic electromotility and drives oscillations in the cell’s length, which occur at the frequency of the incoming sound and provide mechanical feedback amplification. A movie clip showing an isolated outer hair cell moving in response to electrical stimulation can be seen here....
without functioning outer hair cells the sensitivity decreases by approximately 50 dB. Outer hair cells extend the hearing range to about 200 kHz in some marine mammals
From the Abstract:
The paper - using guinea pigs, whose hearing characteristics resemble that of humans, they claim - then goes on to claim that:Normal hearing depends on sound amplification within the mammalian cochlea. The amplification, without which the auditory system is effectively deaf, can be traced to the correct functioning of a group of motile sensory hair cells, the outer hair cells of the cochlea. Acting like motor cells, outer hair cells produce forces that are driven by graded changes in membrane potential.
[ack: He's now describing his new technique using lasers for measuring motility] Long cylindrical cells, such as OHCs from the apical end of the guinea pig cochlea, can be drawn into a suction pipette and stimulated with a current passed down the pipette. The method is noninvasive in the sense that the plasma membrane is not punctured and intracellular contents remain undisturbed even though the suction pipette internal diameter and the cell diameter have to be very closely matched. The technique offers good stability for the recording of cell length changes even though it does not permit the intracellular potentials or currents to be measured directly. The microchamber also permits different solutions to be presented to the apical and the basolateral surfaces of the cell, thus more closely mimicking the situation in vivo. The configuration allows an elegant demonstration that deflection of the stereocilia does indeed lead to the electromotile changes in an OHC, for the projecting stereocilia can be manipulated while motion of the cell body is measured (85)...
This raises some important questions: Does this motility, or lengthening and shortening of OHCs, directly affect hearing up to those frequencies? If it can do it for marine mammals, and as high as 200kHz, why not humans? If we still don't hear beyond ~20kHz as measured by an audiologist, can we still be stimulated by higher frequencies by some other means that affect perception of sound and/or its location? If not, what's the significance of this research finding?Such experiments [ack: Referring to similar but older experiments, using now-considered-limiting techniques using photodiodes] reported that the upper limit of electromotility was above 22 kHz. That higher rates could not be measured more precisely was probably a consequence of the limited bandwidth of the instrumentation, and in that case the photodiode system employed. Such limitations have subsequently been removed and, by enhancing the signal-to-noise ratio of the optical measurement by using a laser vibrometer to measure light reflected from an atomic force microscope cantilever placed on the cell axis, a much higher frequency limit of the electromotility has been determined. The 3-dB point of the frequency response was found to be 79 kHz for cells from the basal, high-frequency end of the cochlea, and at a slightly lower frequency for cells from the apical, low-frequency end of the cochlea.
The paper appropriately asks:
As you can tell, they are not as assertive as Wikipedia...Is OHC motility really the explanation for "cochlear amplification"?
Finally, a few more claims:As Hallowell Davis presciently remarked in 1983: "The mechanism of the CA (cochlear amplifier) is unknown, and the problem remains of how its action can be triggered by submolecular movements near threshold."
From this I take that OHCs directly relate to the auditory nerve (the so-called 8th cranial nerve) , and that there are indeed "nerve receptors up to about 80kHz" if this is what the patent refers to; and the quest continues...Inner hair cells (IHCs), of which there are ~3,500 in each human cochlea, are innervated by dendrites of the auditory nerve and are considered to be the primary sensory hair cells of the cochlea. Outer hair cells (OHCs) number ~11,000 in each human cochlea and lie in 3 or 4 rows... Only 5% of the dendrites of the auditory nerve are associated with OHCs.