Re: HC selectivity ... was Re: Physiological models of cochlea activity - alternatives to the travelling wave

["Richard F. Lyon" <DickLyon@xxxxxxx>]

At 2:44 PM +1000 10/4/07, Andrew Bell wrote:
> The point is that we are talking about the input signal to the cochlear
> amplifier. There has to be a passive signal (the effective stimulus) on
> which the positive feedback process can work. The BM displacement that is
> measured in a normal cochlea is _after_ amplification has occurred (remember
> that AJ's original figure of 1 pm was derived from Ruggero et al. 1997 by
> looking at their post-mortem data).
>
> So the fundamental question is, how can a normal cochlea detect 1 pm and
> amplify it a thousand-fold (60 dB) so that we see a 1 nm displacement? I
> agree with Martin that it can't, and there has to be some other, larger,
> effective stimulus.

Yes, that is the fundamental question, sort of.  It's not like 
there's some element that detects an "input" of 1 pm and amplifies to 
an "output" of 1 nm; rather, there's a distributed amplifier that 
multiplies up the power of traveling waves.  At the low end of the 
range, everything behaves linearly.  As long as the noises of the 
many hair cells are reasonably uncorrelated, the system will be able 
to work to orders of magnitude below the level that would cause a 
"noticeable" effect in a single hair cell.  Ultimately, the shot 
noise of ion channels, averaged over many OHCs, is what will set the 
sensitivity limits; there's no "threshold" below which amplification 
stops working, the signal just gets down below the noise.

So I reiterate: it's a funny strawman to look at what the motion 
would be in a dead cochlea and say that's too little for the OHCs to 
work; they do work, and the result is that the motion is much greater.

Dick