Re: Wasn't v. Helmholtz right?

[Eckard Blumschein <Eckard.Blumschein@xxxxxxxxxxxxxxxxxxxxxxxxxx>]

Dear Andrew Bell,

Thank you for pointing once again squarely to some uncontested facts!

First of all, the traveling wave is an epiphenomenon. Hiding behind v.
Bekesy is not justified. As you wrote, he himself, in one of his later
papers with Wever and Lawrence, acknowledged that the TW could be seen as
merely descriptive of the result of the action of oscillating acoustic
pressure in the cochlea.

Correspondingly, it seems to me overdue asking for practical consequences
as well as for revision of all textbooks dealing with that matter except
the excellent book on Auditory Perception by Richard Warren who already
prepared the reader to this possibility.

Your second important hint relates to the previously enigmatic fact that
SOAE and even DPOAE was reported for animals like the gecko that do not yet
have any basilar membrane but a just tectorial membrane.

We certainly also agree that the OHCs including their stereocilia act as
preamplifier.

However, I am somewhat confused. After you called (on page ii) the
hair-like stereocilia the sensing elements of the hair cells, you wrote (in
your reply) that you considers the body of the OHC to be a much more likely
receptor of acoustic energy.

You are wrong about me: I did never believe that the OHC stereocilia are
the resonant elements. I just wrote "most likely the stereocilia of the
outer hair cells act as the primary sensory elements". I do not share your
view that the primary sensory elements must act as resonators. I merely
guess the OHCs have to react with depolarization to some change affecting
their surrounding by negative (rarefaction) pressure.

Why not considering the tectorial membrane possibly also involved in that
task? You provided an argument for that (on p. 24): TM has the intrinsic
property of impeding sound transmission, resulting in the creation of
appreciable acoustical forces. Could not a very weak rarefaction click open
potassium ion channels located at the tips of stereocilia by lifting the
lip of TM at least at location of the outer row? As soon as this would
cause depolarization of the corresponding OHC, that OHC will shorten and
draw back the from a putative covering fovea located on surface of TM, i.e.
further widen the gap between tip and TM. Efferent innervation could be
required in order to maintain the balance of a delicate mechanical distance
between tip and TM by adjusting the dc level of receptor potential. Such
system would be sensitive against change of static pressure as you
remembered of. Everybody realizes changing static pressure by ear.

BTW, I consider spontaneous firing of auditory nerve fibers the natural
solution which allows to detect displacements down to as little as just one
diameter of a hydrogen atom without relying on resonance. Otherwise, the
OHSc would suffer from the same problem as an A amplifier.

Well, your central concern is the resonant element. I am aware of many
highly qualified specialists who gathered a lot of facts related to that
secondary question. Unfortunately, I am poorly informed. Nonetheless, I
cautiously conclude from ARO abstracts that there might be a rather complex
mechanical interplay indeed, involving reticular lamina, Hensen's cells,
etc. If I remember correctly, fluid was reported to move in radial
direction ten times faster than along cochlea partition. So I am sorry, I
feel unable to comment on your special ideas.

Partially you got me entirely wrong. I never suggested that the stereocilia
convey charges to the TM but would not such transfer make sense the other
way round? What about the IHCs, as far as I know, they do not touch the TM.

As a corollary, I acknowledge your contribution to the revival of the
resonance theory of hearing. Do you really need to additionally claim a
comprehensive model that encompasses the panorama of hearing physics and
psychophysics? I myself would definitely not be able to manage that.

Eckard Blumschein