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

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.