Subject: Re: HC selectivity ... was Re: Physiological models of cochlea activity - alternatives to the travelling wave From: Andrew Bell <andrew.bell@xxxxxxxx> Date: Thu, 4 Oct 2007 18:11:43 +1000 List-Archive:<http://lists.mcgill.ca/scripts/wa.exe?LIST=AUDITORY>Dick: I'm pleased we now both see the 1 pm for what it is: the fundamental input signal of the traveling wave theory at 0 dB SPL. You express faith that such a signal is sufficient to give a 1 nm measurable displacement via a traveling wave mechanism of some sort. Yes, the evidence is that the OHCs do the work, but why do you assume it's via a 'traveling wave' mechanism? There could be other mechanisms, could there not, and if an alternative one happened to give LARGER input displacements than what the TW offers, it would seem to make a better candidate for the effective stimulus. Calling such an alternative a 'strawman' seems a pejorative term that prejudges the issue. If AJ's calculation returned a value a thousand times lower (0.001 pm) would you still have faith that the TW could dig below the noise threshold and take care of everything? In other words, do you have a threshold below which you think the traveling wave mechanism would have insufficient traction? For me, 1 pm is below my threshold of credibility, but I can rest a bit easier with a pressure-induced motion of 100 pm. I have recently published a cochlear model in which outer hair cells produce standing waves in the subtectorial space (Bell, 2007), and in it that 100 pm figure could be used as the input to a local, OHC-driven cochlear amplifier. So the TW need not be the only theoretically possible amplifying mechanism. Bell, A. (2007). Tuning the cochlea: wave-mediated positive feedback between cells. Biological Cybernetics 96, 421-438. Andrew. ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ Andrew Bell Research School of Biological Sciences The Australian National University Canberra, ACT 0200, Australia T: +61 2 6125 5145 F: +61 2 6125 3808 andrew.bell@xxxxxxxx ~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~ -----Original Message----- From: AUDITORY - Research in Auditory Perception [mailto:AUDITORY@xxxxxxxx On Behalf Of Richard F. Lyon Sent: Thursday, 4 October 2007 5:00 PM To: AUDITORY@xxxxxxxx Subject: Re: [AUDITORY] 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. Dick