Talk:Soliton model in neuroscience

Discrepancy?
In reference to a paper entitled On the (sound) track of anesthetics, Thomas Heimburg claims "that no such heat is produced," by electrical impulses as they travel along the nerve. science.ku.dk/ This contradicts what is stated under "Justification" of the Soliton model, which states that it "has been known for several decades that an action potential traveling along a neuron results in a slight increase in temperature followed by a decrease in temperature." Can this be resolved? --Maradja (talk) 10:43, 30 August 2010 (UTC)
 * In experiments on nerves one finds a first phase with positive and a second phase with negative temperature changes during the action potential. The integrated heat over the whole process is zero. See the edits in the article --IBrane 15:52, 7. September 2010 (UTC)

---
 * Actually, the net heat is not zero. The observed temperature changes can be modeled using the HH model. For example, these authors propose that the initial positive  heat is caused by the switching of the HH sodium channels and the later negative heat by the closing of the channels: http://www.pnas.org/content/74/9/3810.full.pdf I don't know  the current state of the literature on this topic, but the claim that the heat measurements falsify the HH model is wrong.


 * The heat argument is invalid, in any case: The HH currents are very definitely present; the membrane capacitance is definitely discharged. Heat is necessarily produced. Calculations show that it is a very small quantity, but it must be there.

MervinFerd (talk) 12:38, 26 May 2015 (UTC)

Serious?
Are these guys for real? How do they explain
 * A)Abolition of the AP by voltage channel blockes
 * B)The fact that APS still occur at higher or lower temperature than normal, albeit with different kinetics?

Dsol 16:17, 1 April 2007 (UTC)


 * sounds like a hoax. Yes they have actually published this idea in a physics journal, but I cannot imagine any neuroscientist taking this idea seriously. Medlat 19:00, 1 April 2007 (UTC)
 * Actually, I skimmed their papers a bit, and it seems kind of interesting. I think the problem is just the way it was presented here and on action potential as an alternative to Hodgkin Huxley.  In fact it's an extension of the existing theory, and definitely does not seem to work without at least some help from ion channels.  If I have time I'll read their papers and correct this, though mainly I'm busy writing my own. :) Dsol 22:26, 1 April 2007 (UTC)

There's an interesting direct response by Heimburg to a question about press coverage of this here:  (scroll down to Question #2). It answers some issues raised here - in particular, he does mean that it's an alternative to Hodgkin Huxley, since HH uses irreversible thermodynamic processes and the soliton model doesn't; they differ on the role of ion channels. Maybe worth linking to. -- anon.
 * OK, so he's saying that the electrical effect in AP transmission is due to capacitance changes in the membrane as it becomes more or less thick. As I understand it, his model of the AP has no active sodium conductances, which makes it kind of hard to explain why the AP vanishes when you block them. The fact that he explains anesthesia somewhat suggests that the truth is that both effects are important. Dsol 18:23, 13 June 2007 (UTC)
 * If you read the "Thermodynamics of..." paper, one section describes how changing the ion concentration affects the melting transition. I'm no biologist, so this is wild speculation, but that sounds like one plausible mechanism for the effect of ion channel blockers? As Heimburg is at pains to point out in the papers and in the response above, thermodynamics just give predictions based on the macroscopic properties of substances, without addressing the underlying microscopic processes -- anon (who will now leave this to the experts).
 * Blocking active conductances such as voltage gated sodium channels shouldn't have any effect on ion concentrations. But in the PNAS paper these guys seem to argue that the effects of canonical channel blockers such as TTX have been misunderstood, referring to a couple of experimental squid-axon studies in the late 60s that have been cited 4-5 times. Time will tell... Dsol 09:29, 14 June 2007 (UTC)

Has anybody found out what triggers the sound pulse/density change or whatever? Gomphaman 11:19, 30 August 2007 (UTC)
 * They don't mention that in their papers, and I imaginge that's the first thing a skeptical electrophysiologist would ask. I guess they would answer that current or charge is somehow responsbile for the pulse initiation. Dsol 19:21, 30 August 2007 (UTC)

I really don't understand what's going on with the people supporting this model. Even if there is some interesting phase transition stuff going on in the lipid bilayer (and maybe there is--I'm no expert on that), they can't just discount the mountain of data on ion channels collected over the past few decades. Plus, there's no obvious reason their model necessarily contradicts the HH model. For example, it has been demonstrated that hydrophobic small molecules that partition into the membrane, altering membrane stiffness, etc., alter the gating properties of voltage-gated channels. Maybe someone should add these points to the main page.Evilrobotxoxo (talk) 01:34, 9 December 2007 (UTC)


 * They never say that they want to overthrow HH - their model simply says that a soliton can form and will form if a voltage spike occurs consistent with that predicted by ion flows in HH. However, the work on anesthesia and the very small irreversible heat loss that has been measured suggests that the ion channel mechanism A. may not be the primary source or first cause of the neuron spike and B. may not be effectively modelled by a resistor. HH voltage spiking occurs - nobody can deny that. They are again saying two things: that the voltage spike may not be the primary means of signal propagation and that the circuit model may not be the best to describe ion channels. SamuelRiv (talk) 02:19, 9 December 2007 (UTC)


 * Their papers never spell out that they think HH is wrong, but they're just being coy: I know they have said in other places that they do believe that their model is an alternative, not an extension to, the HH model. I don't remember where I read or heard this--it may have been in the Skeptic's Guide episode listed above.  From my perspective as an experimentalist, there are a few serious problems with the soliton model.  If the membrane really is perched at the brink of a phase transition, how can APs propagate over such a wide range of temperatures?  This isn't just some in vitro observation--if you put a vial of fruit flies in an incubator at say 12C, they will crawl slower, but they'll still crawl around.  If you move them to an incubator at 37C, they'll move faster.  How is that consistent with solitons being the primary mechanism of AP propagation?  Another problem: blocking channels blocks APs.  And not just through vague membrane-binding mechanisms, I'm talking about channel blockers that have been crystallized in complexes with specific ion channels, so we know exactly where their binding site is.  Or other ones that haven't been crystallized, but where you can eliminate binding with point mutations of the channel.  As far as the anesthesia stuff goes, the whole meyer-overton thing is simply not evidence for solitons.  The primary basis of that is blood-brain barrier permeability and bioavailability, not actual efficacy at a given concentration.  Also, there has been plenty of in vitro work supporting more traditional interpretations of anesthetic action, and there has also been in vivo imaging work showing effects of gas anesthetics in the parts of the thalamus that lead to minimally-conscious or vegetative states if lesioned in humans.  It all fits.  I don't personally know much about the whole temperature shift thing, but even if that's entirely true, it seems to me that reflects some interesting phenomenon going on in the bilayer that's simply captured in the curve fitting of the HH model.  No one knows the exact mechanism by which voltage-gated cation channels do their thing, and it seems likely to me that interaction with the bilayer is likely to be an important part of it, especially considering that bilayer stretching forces and membrane composition have been shown to have strong effects on channel gating.  But that's getting at the mechanisms of how channels work, not the mechanism of how something other than channels underlies the AP.  As a final point, how does the soliton model explain bursting and related phenomena?Evilrobotxoxo (talk) 15:41, 9 December 2007 (UTC)


 * If you listen to the Skeptic's Guide episode, some panelists object to the idea of overthrowing a well-established model, but the one who actually corresponded with Heimburg said that he emphatically did not intend to overthrow the model - the idea was misshapen by the press. The episode made a good analysis however, in that it really does seem to be a clash of disciplines going on here. In biophysics, the circuit model is standard for analyzing neurons (note the circuit model refers to any of the popular ones models that use ion currents as their principal mechanism, the most robust being HH). In experimental biology (for which I worked in a lab once) the actual physics wasn't a concern so much as that the model fit data extremely well. This is all fine, but in physics, we care about getting the mechanism, cause, and effect right, with models derivable as much as possible from first principles. If a model works then it works, and you can use HH all you want and no physicist will object. But what biophysics objects to is the inconsistencies of the model with experimental data (again, the heating-cooling effect has been observed in both vertebrate and invertebrate CNS), and in physics what usually happens is a new model is presented that only explains a small defect in the established doctrine, but might not explain everything that the establishment explains. That gets a few of us excited, and we extend the model until we have a viable competitor or we find the model predicts the established model exactly. If the latter occurs, then we're done, but if the former occurs, we establish regimes at which each model is viable, make appropriate guidelines, and continue working to extend and unify. This is exactly what happened with general relativity and quantum mechanics when they were introduced. The soliton model may still be wrong - it's too young to tell - but at no point will it "overthrow" HH, and the authors know that. SamuelRiv (talk) 18:30, 9 December 2007 (UTC)


 * I don't remember exactly what was said in the Skeptic's Guide episode, and I don't have time to listen to it again, but I do remember reading or hearing direct quotes from them saying that they thought that the HH model was basically wrong. Maybe they have backpedaled from that stance.  When I first heard this idea, I was like you--I thought it was a really interesting extension to the HH model.  But their evidence was just so weak--the whole anesthetic action thing, which is interesting but IMHO misinterpreted, and the whole temperature of phase transitions that so glaringly can't explain why action potential propagation is robust across such a wide scale of temperatures in vitro and in vivo.  How do you reconcile those things with their model?  At what point does it switch in your head from being an interesting idea to a sloppy idea?  Look, I think there is a lot of interesting stuff going on in terms of interaction between the channel and the bilayer.  We even have crystal structures of a voltage-gated cation channel now (the guy who solved it was on my thesis committee), but we don't know how that structure generates the observed dynamics.  What I'm saying is that even if the soliton model is completely correct, it wouldn't overthrow the HH model, or really even be an extension to the HH model.  It would be another model at a finer resolution scale that would provide greater insight into where some of the fit-to-data terms in the HH model come from.  This is not the same thing as replacing classical mechanics with relativistic models.Evilrobotxoxo (talk) 15:01, 10 December 2007 (UTC)


 * I meant that it is the same historical pattern with any revolution of a well-established model in physics. A new model only explains a small problem, and in doing so explains some other little thing, and may not explain everything else. Then it attracts interest from other physicists who extend the model, and if it is successful, then it proves to be some specification of the former models. All I'm saying is that a new physical model cannot be dismissed offhand if it is based on sound first principles and successfully fits some data. Theoretical physics isn't the same field as experimental biology, so please don't hold it up to the same standards of viability.
 * And again, they never claimed to overthrow HH - what you saw was something in the popular media that stretched their claims (also, Heimburg said that the university admins handled press releases, so the university may have made a mistake as well).
 * Finally, note that the phase transitions in the membrane are not a single melting point, but a variable specific heat peak over nearly 50K of temperature. See the graphs on their paper. The claim (I think) is that homeostasis is set very near the highest peak to maximize soliton propagation speed. SamuelRiv (talk) 16:22, 10 December 2007 (UTC)

Memristor
Could someone explain why the memristor article is linked to from the bottom of the soliton model article? What is the connection between the two concepts? There is no allusion to a connection within the soliton model article and I cannot find any information about the connection on the memristor article either. Please clarify.

--BBUCommander (talk) 16:44, 17 April 2009 (UTC)


 * It has now been a month and no replies have been given. Thus I will remove the memristor link.


 * --BBUCommander (talk) 17:40, 20 May 2009 (UTC)

Mark as needs expansion?
I read their 2005 article not long after it was published and just today stumbled upon this wikipedia page. I never thought to check to see if there was one. Reading the article for the first time today I found it mostly a response to, rather than a summary of, the theory. I would like to see a bit more description of the model itself at the top of the article. Sorry for not logging in. 64.114.134.52 (talk) 20:59, 10 December 2010 (UTC)

65.185.121.96 (talk) 12:48, 12 May 2015 (UTC)

This is a fringe theory. Flag as controversial or delete
This is a fringe theory and needs to be marked as challenged for impartiality.

A note already present lays out a number of objections, but the theory is too 'far out' to have merited much rebuttal in published sources. There is a single publication in a refereed journal. The theory has not received attention or support in the neuroscience community.

Flag as controversial, or delete. 65.185.121.96 (talk) 12:51, 12 May 2015 (UTC)


 * I strongly support this suggestion. See WP:FRINGE, especially:
 * '''"A Wikipedia article should not make a fringe theory appear more notable or more widely accepted than it is."
 * I agree as well, it should be clearly mentioned at the beginning after the initial introduction that only few researchers are actively working on this theory and its not a mainstream idea in the field.

'''
 * The article presents itself as an alternative to one of the central tenets of neuroscience, without noting that it appears to be a pet theory of a few researchers, and has failed to gain any traction in the wider community. For those coming from outside the field, I'd say the situation is roughly analogous to a theory proposing to be an alternative to the idea that DNA carries heritable information.
 * It has been 10 years since the 2005 paper from Heimburg so I would not make a judgements regarding the traction this research is generating. For those who have read up on the research more closely the difference is not as stark as been pointed out here by the DNA example. The theory provides a different perspective (macroscopic vs molecular) and a more appropriate comparison (analogy) would be  its the peak at 90degC in the calorimetric data of a nucleus (corresponds to denaturing DNA) that carries the hereditary information and not the one at 60degC or 20C (corresponding to protein denaturation and lipid melting respectively). Now one can call it an alternative theory but this is clearly not the case.


 * Others on this page have done a good job of pointing out the weaknesses of the hypothesis (as has Tom Nickoll over at Quora: []), but Wikipedia, and talk pages, are not the place to debate the merits of the theory itself. Rather, we should determine whether the theory is notable enough to merit its own article (I'd vote no), and if so, should attempt to place the hypothesis in its proper context so as not to mislead readers into thinking it is something other than a fringe view.
 * The write up by Tom Nikoll is such a mess (and he has done the same to this page) that it will take enormous effort to correct and convince him for which I don't have the time. Following every statement by "soliton model has no explanation for it" does not make for a good critique. Whatever follows are conjectures (by a contributor to this wiki article and not from any citable resources) based on his/her limited understanding of the thermodynamic approach. For example temperature pulse is a clear contradiction and all the papers he has cited also support it. The issue is not that should there be a temperature pulse or not. "Cooling argument" does not imply "only below baseline" drop but also in-sync drop in temperature and voltage from the peak value. The papers that have been cited only explain the rise in temperature quantitatively and not the drop. There has been a sly attempt to present capacitive cooling as an explanation in the wikipedia article here where as none of the articles cited in support make such a definitive (or quantitative) claim and its only a conjecture by a contributor to this article. Claims regarding toxins and specific agents are explained by perturbation in critical point (Tasaki). Claims regarding wide temperature range is explained by adiabatic state diagram (phase transition is a line and not a point for a nonlinear wave). The propagation in soma vs axon can be explained by local changes in compressibility (the mainstream community already explains several such features using variable density of ion channels in soma vs axon) etc. There are many such subtle aspects which no one has time to go in detail on a Wikipedia page. In fact this wikipedia article grossly misrepresents the thermodynamic approach. With regards to the fate of the article, weather an article is on wikipedia or not does not decide the scientific legitimacy of a research field so I am completely ok if this article is removed. However I certainly mind the present state of the article.


 * I'm not enough of a wikipedia maven to know the best way to steer this through what seems likely to be a contested editing/deletion process, but I wanted to register my support for such an action here.


 * I would suggest that the article be drastically shortened, in case it is kept, with only an introduction and few references to the original research articles. This followed by a disclaimer that this is not a mainstream scientific theory, making no judgements regarding its correctness (that should be left to the reader). Sections regarding justification, formalism, discrepancy, role of ion channels etc should be removed.


 * Cheakamus (talk) 20:14, 19 January 2016 (UTC)

Substantial changes to correct false information and uncritical tone.
The 'Soliton model' is a naive theory which is contradicted by a 65 years of quantitative and qualitative data. The action potential is one of the best-studied and best-understood phenomena in biology; the 'soliton model' is supported by a single refereed paper. It has generated no support in the neuroscience community. The original article treats this fringe theory as a serious challenge to the accepted Hodgkin Huxley model. This is seriously misleading and false. — (talk • contribs) 02:58, 17 May 2015 (UTC) MervinFerd (talk) 03:06, 17 May 2015 (UTC) MervinFerd (talk) 17:03, 26 May 2015 (UTC)


 * I agree with your comments regarding impartiality and uncritical tone and the article should be formulated so that it's controversial nature is clearly evident, it can also be placed under the Wikipedia's scientific controversies category. But Wikipedia is not a place to settle scientific debates rather its for dissemination of information and any subjective claims that are not supported by peer reviewed articles should be removed. The article should not be removed or censored just because its controversial.


 * Second regarding the model, the complete framework that combines nonlinear acoustic and thermodynamics of membranes does not contradict any of the 65 years of experimental data on nerve impulses, no scientist in their right mind would pursue a theory where 65 years of data already existed that       . The theoretical framework provides alternate explanation for many of the observations that are listed as contradictory and remains open for others that are yet to be shown and a lot of research needs to be done both theoretically and experimentally. The model does account for ion current however it does not require to classify them as sodium or potassium current etc. The model also provides a clear explanation regarding the initiation of sound waves via nonlinear photo-mechanical, chemo-mechanical or electromechanical couplings intrinsic to membrane systems. Finally while the hydrodynamic equations that model solitary pulses won't have explicit terms for every possible chemical and physical cue out there (which is a good thing), all those effects are implicitly present in the state equation (for example c_0, p, q and h in soliton model) and are analyzed separately using thermodynamics.  The selectivity to any of these cues comes from the highly nonlinear nature of the state equation which is sensitive to small perturbations in for example ion concentrations, pH or toxins etc. Geometrical factors make for boundary conditions and primarily factor in parameter h in case of solitons. Again note that soliton is a particular solution of nonlinear wave equations which come in all shapes and sizes and depend on many thermodynamic and geometric factors that can explain the wide range of shapes observed for action potentials in different systems.  50.14.40.49 (talk) 13:31, 21 May 2015 (UTC)

———————


 * Heimburg is very clearly pushing the model as an alternative to Hodgkin Huxley. He is coy about it sometimes, but that is clearly the point.


 * "The theoretical framework" may provide explanations, but can you apply them to an actual neuron? That some particular combination of membrane properties might explain some aspect of some action potential is not useful or serious.


 * "The model does account for ion current however it does not require to classify them as sodium or potassium current etc. " WHAT? Ionic substitutions and drugs that target specific channels are the core of neuroscience (and medical applications of neuroscience). Any theory that does not contain these elements is false on its face. Such a framework "contradicts the theory even before its conception."

MervinFerd (talk) 17:02, 26 May 2015 (UTC)


 * You have clearly made up your mind and refuse to understand anything that is outside the scope of Hodgkin and Huxley model. A new theory by default doesn't agree with the old theory, it only agrees with the old experiments (and not their interpretation based on the old theory)as simple as that. So you can't use the argument that because it doesn't agree with the old theory its wrong. Hodgkin himself raised it many times that the model is not supposed to be taken literally, even later in his reviews. He was also conserved about the nature of temperature pulse (1975 review). The currents are only interpreted as sodium and potassium fluxes and when an agent affects the wave front it is assumed to have blocked sodium channel and if its the wavetail it is assumed to have blocked the potassium channel because in Hodgkin and Huxley model front and tail are explained by sodium and potassium channel respectively. Please provide references where selective fluxes of sodium and potassium have been directly observed during the action potential. The effect of sodium or potassium or for that matter any ions or drugs are explained in the thermodynamic theory by their effect on the state nonlinearities (read many references in the papers of the proponents of this theory). Scientific hypothesis are made to be proven wrong and you should not get sentimentally  attached to them. You have taken over the whole article before discussing your changes here and now no one has the time to correct that. Hodgkin and Huxley model is a great intuitive model where the membrane was reduced to a circuit because APs were being measured electrically. However a complete theory needs to derive the action potential wave equation based on first principles, that is conservation of mass, charge, momentum and energy, none of which (except maybe charge) was done by Hodgkin and Huxley. Heimburg and co have made first attempt in that direction. This doesn't take any credit away from Hodgkin as he clearly knew what his model is good for.

Coming to your specific objections thermodynamic model doesn't say that there can't be a heat production or dissipation during sound wave, what do you think happens during shock explosions or tissue ablation using ultrasound. In fact the thermodynamic model can account for both single phase and biphasic heat pulse coupled to action potential while Hodgkin and Huxley cannot even explain one of them because if the heat is released as a result of dissipation the temperature cannot even fall in sync with voltage let alone go below baseline. By the way one does not calculate heat dissipation using your formula for a reversible process, think of a capacitor circuit without a resistor inside which a dielectric oscillates. The dielectric will oscillate forever without dissipation even though you have current in the wire connecting the two plates of the capacitor. I can go on and explain each and every objections but the truth is the thermodynamic model is not completely developed and there are lots of interesting things still to be explained but so far the indications are promising and there are no fundamental contradiction in the thermodynamic models and the data on nerve impulses. Its an exciting new field and new people will join eventually after there is sufficient evidence. — Preceding unsigned comment added by 192.76.7.170 (talk) 15:15, 19 June 2015 (UTC)

--- Mervin Ferd   reply to anonymous above 1. Heat

It is simply false that the HH model cannot explain the observed heat. All the authors working in this area interpreted their results in term of the HH model. The HH currents are not a dielectric moving in a vacuum; they are ionic currents flowing through resistances; they produce a predictable heat. The negative heat (decrease in temperature) can be explained either by K+ ions moving with their concentration gradient but against the voltage gradient ---entropy of mixing--- or by configuration changes in the membrane (increased entropyheat releasedduring depolarization followed by decreased entropy heat absorbed on repolarization.

As this is the only argument in favor of the model, it is weak, indeed.

2. "Please provide references where selective fluxes of sodium and potassium have been directly observed during the action potential." Please read the original HH papers. It's all really very clear. The literature from the last 60 years is enormous. At this point we have not only the selective fluxes, but the gating and selection mechanisms worked out to the molecular level.

The proponents of the Soliton Model display an incredible ignorance of even the most elementary neuroscience.

3. " I can go on and explain each and every objections but the truth is the thermodynamic model is not completely developed" On this, we are agreed.

4. If you can answer any of the points of disagreement between the soliton model and experiment, I will cheerfully remove them myself.

MervinFerd (talk) 00:06, 13 August 2015 (UTC)

Too many speculations and the article has been vandalized
Wikipedia is not a place for original research. The section "Differences between model predictions and experimental observations" is full of speculations about soliton model by someone who has not even tried to understand the model. Its just too much effort to correct the article at this point and may be the article should be deleted as was previously suggested, not because it represents a fringe theory but because it has been vandalized massively by someone who has too much time. — Preceding unsigned comment added by 72.221.92.113 (talk) 02:42, 24 May 2015 (UTC)

The article has not been vandalized; false and misleading information has been corrected
The article has not been vandalized. The section "Differences between model predictions and experimental observations" simply points out obvious difficulties that render the model indefensible. Any person with an undergraduate understanding of neuroscience will see these difficulties immediately.

If proponents of the model think these objections are not valid, then refute them. Wikipedia is not a place for original research; but, it is also not a vanity press for publicizing eccentric theories.

The model -is- fringe science, verging on Crank. It was advanced by a credentialed scientist, but after a decade has received no notice or support in the neuroscience community.

The original article treated this crank science as a significant challenge to the universally accepted Hodgkin Huxley model of the action potential. The Hodgkin-Huxley model is at the base of Neuroscience; accepting this model requires disregard of (literally) thousands of careful experimental and theoretical publications.

I concur that the article should be deleted---because it glorifies an hypothesis advanced in only a small number of refereed publications and having no support beyond its original authors.

However, under no circumstances should this silly, naive hypothesis be presented as a legitimate challenge to the Hodgkin-Huxley model (and the whole of neuroscience).

--- Note: there are thermal and mechanical changes associated with the action potential. Study of these phenomena is entirely legitimate and may be a significant supplement to the accepted model. However, although model proponents fudge the issue, the published documents clearly show that the model is intended to replace Hodgkin Huxley, not to supplement it.

Note: I agree that further citations are needed. The original article was too heinously false to leave in public view. -

MervinFerd (talk) 03:29, 24 May 2015 (UTC)

Definition of the soliton model as originally posted
The anonymous commenter claimed that I had not even tried to understand the model. Here is the description of the model in the original article, which has been changed, not entirely by me:

"On the other hand the soliton model ( and sound waves in general) depends on adiabatic propagation where the energy provided at the source of excitation is carried adiabatically through the medium, i.e. plasma membrane. Indeed it was the measurement of a temperature pulse and the absence of heat release during an action potential, measured and repeated in several systems [3][4], that seeded the initial ideas of nerve impulses being an adiabatic phenomenon much like sound waves. In particular it was the active cooling during a nerve impulse that contradicts the Hodgkin–Huxley model. To be specific the soliton model is concerned only with the propagation of nerve impulse and not with its excitation (i.e. action potential)."

This more recent writing clearly states that the HH model is false and is to be replaced by the Solition model: Advances in Planar Lipid Bilayers and Liposomes 16: 275-299 http://www.membranes.nbi.dk/pdf/2012_AppalivanRienenHeimburg_APLBL.pdf#
 * ''' "Taking the reversible heat of the nerve pulse serious, one is inclined to state that the HH model in itself cannot be correct. The same argument would hold for a combination of both models. Thus, it seems necessary that any protein-based picture would still operate on the basis of reversible processes, for instance, by employing capacitive currents rather than ohmic currents, that is, by transporting charges forth and back in a reversible process. This implies that the HH picture cannot easily be combined with reversible physics and the soliton model without seriously changing its mechanism."--pg 295

'''

The essential feature of the hypothesis is 'adiabatic propagation', like a sound wave. The published sources don't get more specific than that. But, taking that as the essential of the hypothesis, the obvious question arises:

"From whence comes the energy to spread the excitation from the axon to the very much larger surface area of a soma."

I listed a number of other obvious objections in the disputed section, but this one is the easiest to explain to someone not familiar with the field.

'''The claims about heat generation being incompatible with Hodgkin -Huxley are false. See, for example: http://www.pnas.org/content/74/9/3810.full.pdf'''

Note also that there is no mechanism of generating the sound wave.

MervinFerd (talk) 12:43, 24 May 2015 (UTC)

Reverted to previous correct statement that observed temperature changes are consistent with HH
Some proponents of the 'thermodynamic' soliton model seem not to be well versed in thermodynamics. The 'adiabatic' cooling/heating cycle is consistent with some process resembling a phase change that reverses as the wave passes. I cited a paper (http://www.pnas.org/content/74/9/3810.full.pdf) that attributes this change to opening/closing of the HH sodium channels, but other changes would work as well.

But, the heat argument is fundamentally invalid. The HH ionic currents are undeniably present; the membrane capacitance is undeniably discharged; these processes must produce heat. That is basic physics. Some studies observe this heat, some do not; these are very difficult experiments.

(The energy stored in a capacitor (Joules) is : 1/2 CV^2. Assume V = 0.1V, C = 1 microfarad/cm^2)

MervinFerd (talk) 01:20, 30 May 2015 (UTC)

Broken sentence in first paragraph
Here's the sentence:  "The model is proposed as an alternative to the Hodgkin–Huxley model[2] in which action potentials: voltage-gated ion channels in the membrane open and allow sodium ions to enter the cell (inward current)." What is the colon following the word "potentials"? It seems to imply a verb; however, what is the verb in question? The general reader wants to know.--75.164.155.194 (talk) 02:49, 28 July 2016 (UTC)