Comments on: Critical Sensation

By: Osame Kinouchi

Osame Kinouchi — Wed, 26 Jul 2006 15:39:08 +0000

Nice comments… Thanks econgeek, we tried, my friend, we tried…
Taion is right in the sense that the link to the retina results is not quit direct because of the complexity of the retinal network. Interesting that Taion, which seems to be a retina specialist, points that the amacrine network plays a structural role similar to the olfactory glomeruli. We hope that experiments in the olfactory glomeruli would be more direct.
Thanks to Cosma for the nice review. Unhappyly, Cosma, the model is, hummm… somewhat over-universal: directed bonds instead of symmetrical ones also works… and sometimes gap junctions are assymetrical also.
Of course, sensory systems are very adaptative, and their dynamic range is very large, with several mechanisms working together. Our proposal is more modest: to explain the dynamic range of the olfactory glomeruli, not the entire dynamic range of animal olfaction. But if Stevens psychophysical exponent would be, if not determined, at least affected by the value of directed percolation exponent, it would be nice, isn´t?

By: beajerry

beajerry — Tue, 25 Jul 2006 14:07:58 +0000

The whole is greater than the parts?

By: Ken C.

Ken C. — Tue, 25 Jul 2006 12:47:27 +0000

The explanation I remember for wide dynamic range involved lateral inhibition: spikes in one cell inhibit spikes in nearby cells, so that a kind of spatial derivative is computed. No?

By: mitch

mitch — Tue, 25 Jul 2006 08:13:42 +0000

As Eudoxis said, I believe there is adaptation occurring within a cell to shift its linear response range. Something I have seen recently (I know there's more, i'm just tired at the moment), I'm pretty sure this retinal model uses such adaptation techniques.

By: taion

taion — Tue, 25 Jul 2006 07:48:01 +0000

I think part of the reason might be that the paper has some flaws—consider “Our results are
consistent with the reduction in sensitivity, dynamical range and synchronization recently observed in retinal ganglion cell response of connexin-36 knockout mice [28].” If you actually look at the reference, you’ll note that while C36 KO mice don’t have the gap junctions among AII cells that might presumably enable those cells to act as an excitable network, they also lack the gap junctions between the AII cells and the appropriate retinal ganglion cells from which the measurements were taken. This essentially means that the RGCs from which the measurements were taken get no signal at all from rods, which lead to the observed effects on the dynamic range/&c. regardless of the excitable network properties of AII cells.

Why do I sound so bitter about this? I’m currently working on a biophysical model of mammalian retinas (cone pathways only though!), and this paper made me spend the entire day chasing around references believing that I’d made a crucial omission that I didn’t. I guess this is what I get for reading CT when I should be working, though!

By: econgeek

econgeek — Tue, 25 Jul 2006 03:58:18 +0000

Why on earth is this appearing in NP instead of plain old Nature. It definatly seems Nature worthy to me. (I am not a biologist but I have seen much less interesting work than this in my field (economics) published in nature or Science.

By: cosma

cosma — Tue, 25 Jul 2006 02:38:21 +0000

Slocum: That’s a good analogy, and I wish I’d thought of it. Kinouchi and Copelli do indeed assume that the signal is encoded in the amplitude. They’re also assuming rate coding, rather than just time-coding, but my understanding is that this isn’t a bad assumption for the early stages of sensory processing.

Eudoxis: Yes, a more realistic model would definitely have to incorporate mechanisms for adaptation. (A slow fall in the susceptibility to external input suggests itself.) This would make for an interesting follow-up paper…

By: eudoxis

eudoxis — Tue, 25 Jul 2006 01:59:07 +0000

There must be multiple mechanisms of adaptations that work on different time scales. For vision, for example, there is a slower, physiologic, adaptive response to stimulus involving modulation of GABA receptors.

By: Slocum

Slocum — Tue, 25 Jul 2006 01:15:37 +0000

I’d suggest that a possible analogy would be ‘the wave’ at sport stadiums. Each person standing and then sitting back down is equivalent to a neuron spike. If each standing person tended to result in, say, 2 standing persons, before long, everybody in the stadium would be standing. If each standing person resulted in fewer that 1 standing persons, in time, nobody would be standing. With a branching factor of 1, on average, the wave persists indefinitely. Makes sense.

That’s simple enough—but where’s the dynamic range? Is the strength of the signal encoded in the amplitude (which would correspond to the percentage of the crowd that is participating in the wave)? Yes, my question would probably be answered by reading the paper, but…

By: John Quiggin

John Quiggin — Tue, 25 Jul 2006 00:30:16 +0000

As a general way of looking at this, is it helpful to make the (trivial) observation that for optimisation problems lacking interior solutions, the objective will be maximized (if at all) at the boundary of the domain? This would lead me to look at expressing the problem in a way that permits the use of convex analysis.

By: NL

NL — Tue, 25 Jul 2006 00:24:54 +0000

To be fair, NP is a brand-new journal, and many places simply haven’t gotten around to subscribing yet.