Yes, this is a contested theory, but it's not a crackpot theory. I'm well aware of the fluid mosaic model. It is not mutually exclusive with what I've described, in fact it's the base from which this theory is formed. And it is not my theory, but the theory first formulated by literally the guy that discovered the mechanism of action of myelinated action potentials (Ichiji Tasaki, who worked on it during his entire time at the NIH). Call it crackpot if you want but please don't do so just because you've misinterpreted a a short forum post trying to introduce a complex concept in a concise way.
To clear it up for you, the transfer of ions across the membrane by ion channels is not something I'm debating. Nor am I saying that the electrical field isn't required for the action potential to propagate. If you took that away from my post I can understand you thinking it's crackpottery. I'm just saying it's not the whole picture. When there's lots of light gas anesthetic dissolved in the lipid membrane keeping the heat capacity low (disordered) it is thermodynamically harder (requires more energy) to form the organized 'solid' (actually more like a gel to be pedantic) state that propagates with/as the action potential.
All these things are happening together, and more (like, how the lateral pressure profile might link the lipid state to ion channel conformational changes, etc). Simple electrical models cannot explain reversible uptake and release of heat (resistance cannot do this) with the passing of the action potential. Nor the reason atmospheric pressure changes dosage, nor the reason there's a change in optical birefringence and scattering. So you know what it describes is not the full picture. But don't take my word for it, go read Tasaki or Heimburg's work on this if you want to understand the detail. http://erewhon.superkuh.com/library/Neuroscience/Lipid%20Mem...
To clear it up for you, the transfer of ions across the membrane by ion channels is not something I'm debating. Nor am I saying that the electrical field isn't required for the action potential to propagate. If you took that away from my post I can understand you thinking it's crackpottery. I'm just saying it's not the whole picture. When there's lots of light gas anesthetic dissolved in the lipid membrane keeping the heat capacity low (disordered) it is thermodynamically harder (requires more energy) to form the organized 'solid' (actually more like a gel to be pedantic) state that propagates with/as the action potential.
All these things are happening together, and more (like, how the lateral pressure profile might link the lipid state to ion channel conformational changes, etc). Simple electrical models cannot explain reversible uptake and release of heat (resistance cannot do this) with the passing of the action potential. Nor the reason atmospheric pressure changes dosage, nor the reason there's a change in optical birefringence and scattering. So you know what it describes is not the full picture. But don't take my word for it, go read Tasaki or Heimburg's work on this if you want to understand the detail. http://erewhon.superkuh.com/library/Neuroscience/Lipid%20Mem...