Neuron; A Simpler Theory

[bernard]

Hi SomaSimplers,

This is perhaps the most important paper that I wrote in these last years.

Neuron; A Simpler Theory (http://www.somasimple.com/pdf_files/neuron_simpler.pdf)

If you do not understand a part just ask.

Hope that you'll like it?

:!: The file is long > 800K, :oops:

[Diane]

Wow Bernard, you've been busy! A lot of it is still over my head, but I like the gist of it, and the art is great. The English could use a bit more clarity. These are just bugs, I'm sure... Are you going to submit it somewhere?
Diane

[bernard]

Diane,

It's only a first draft version and I found bugs, too!

Neuron; A Simpler Theory (2) (http://www.somasimple.com/pdf_files/neuron_simpler_02.pdf)
(some bugs corrected)
Clarify is a necessity but I'm waiting for you? :lol:

ps: About submitting somewhere: Just impossible since the majority of journals ask for 1500$ for each color picture. I'm just a PT, not Bill Gates.

[nari]

I've printed it out, Bernard, and will read it through whenever I can.

Publishing is a formidable process - so I hear - in terms of cost.

Can you start somewhere less costly? I'm not sure what to suggest, as I am not familiar with resources in France.

The illustrations look very good.

Nari

[Diane]

Bernard, I'll do what I can to help you with the English, but I feel like I should understand the entire world of thought that you are entering here, and I don't. Someone with a better grasp of the subject matter would be able to help you a lot more easily with this project. I wonder if Chris (Davia) might be a better helper (if he has time.) Meanwhile, it will be a laborious sentence by sentence adventure, with many emails flying back and forth, but I'll work away at it with you between my other projects.
Diane

[bernard]

Can you start somewhere less costly? I'm not sure what to suggest, as I am not familiar with resources in France.

SomaSimple is a very good place and have a better audience than many French journals. :lol:

...but I feel like I should understand the entire world of thought that you are entering here, and I don't.

Where are you lost with the paper?

[bernard]

Here is a branching showing a known problem encountered by old models;

http://www.somasimple.com/images/axon_cut_03.gif

It is a branching on an axon and these branches have normally different sizes thus with same ionic concentrations, we have diferrent resting potential and action potential and a huge difficulty to plug the branches to axon.

The little branches have same ionic concentrations, different action potential, different resting potential but wired without any problem to the larger portion. It is absolutely possible if we consider only concentration by surface unity and it gives automatically an amplification of APs.

HH models is obliged to solve the riddle by parts because there is electrical conflicts! :wink:

[bernard]

Ion concentration = number of ions or molecules by volume unity
Gradient concentration = ratio established between ions concentrations intracellular/extracellular.
Action potential and resting potential are actually based upon gradient concentrations.

In the previous picture, B1, B2 and A have the same gradients since they contain the same number of ions per unity of volume.
But, when we are measuring amplitudes and voltages, we are using an electronic multimeter that adds all present ions at B1, B2 or A. Thus, because a multimeter doesn't care for volume, there is a summation of all particles that says: Amplitude of resting potential (or action potential) at sites B1, B2 and A are different!

That's just false since if concentrations are equal, amplitudes must be equal.

Amplitude of resting potential (or action potential) at sites B1, B2 and A are equal if we consider the surface/volume of application.

[bernard]

http://www.somasimple.com/images/axon_cut_04.gif

Here another view of problem!
Increasing linearly the diameter of axon without changing gradients induces automatically an increased amplitude.

[bernard]

Here is the traditional view about neuron.

The Nerve Impulse (http://www.somasimple.com/pdf_files/TheNerveImpulse05.pdf)

The file is > 5Mo :oops:

[nari]

Bernard

Your English is great, but I am lost in the figures. :roll:

It's like swimming at night - good feeling, but have no idea where I'm going. My mother topped the state in mathematics and stuff but forgot to pass on the link...

nari

[bernard]

Nari,

Please could you give the figure# so I will explain it with some other words.

[bernard]

http://www.somasimple.com/images/free_endings_glass.png


This one is for nari and concentrations.
All glasses contain the same wine and thus the same percentage (concentration) of alcohol but because the glasses have different sizes thus I have a different quantity of alcohol in each glass.

It is exactly the same with nerve fibres. If you look at A you see a little glass but in C a tall one but they have however the same percentage. Since we are seeing diferent quantities we think automatically there is a different alcohol.

[bernard]

http://www.somasimple.com/flash_anims/ap_01.swf

[bernard]

http://www.somasimple.com/flash_anims/soliton_06.swf

This one shows a travelling AP and 2 spots "moved" by it. They are sites of recording and we can see there is a relation between past and future events.

In that case, it is possible to compute the future events continously (the older theory can't).

[nari]

Bernard

Amazing graphics...the dynamic diagrams are useful, because I am very visual and I need to visualise stuff! (Which is why I am not a scientist)

I have heaps of reading to do at present (including British Columbia!) and your theory is amongst the pile.....all I need to do is read it carefully and switch on some more neurons.


Nari

[bernard]

:!: Attention:
In the travelling animation, the representation of AP is inverted. It is normal and indispensable. It is the static recording (actual one) which allows the turnaround of the curve.

[bernard]

Hi SomaSimplers,

Here an email from a physicist (cited in references).

Hi Bernard,

I just read your email and paper, it is very
interesting. I found some very good thinking in the
paper. As a physicist, I think the only way to promote
these theories is to find an experimental evidence in
their support (at least in some cells). I contacted a
lab at MIT some time ago but they did want to get
involved, and these days I'm busy with other projects.
Maybe there are labs in France that could make an
experment trying to find these phenomena? That could
bring a solid proof to either your or my way of
thinking about it, I can't say who is right without an
experiment. Anyway, its good to know there are people
doubting this old adhoc theory. Good luck in your
work.
Best regards,
Marat

[nari]

Bernard

Great to get a response! Is there somewhere in France you can key into and present your theory?
Hope so

Nari

[bernard]

Nari,

Before I will try to explain in a simpler way the theory and/or creates a working model?

[bernard]

Hi SomaSimplers,

Here are some movies showing the torture intended to axons. It becomes more understandable that such treament may be far from a normal functioning?

Experiments movies (http://www.science.smith.edu/departments/NeuroSci/courses/bio330/squid.html)

[bernard]

A Critical Reexamination of Some Assumptions and Implications of Cable Theory in Neurobiology

[Chris Davia]

Once again I must thank you, Bernard, for directing people to my work. Also, Dianne - for overestimating my abilities.

I am sorry not to have been able to join this discussion sooner. I have been very busy. My PhD RC committee meeting came up and it seems that I must do some work. - Goodness! What is the world comming to?

There is something about me that I don't think that you realise, Bernard. I am not formally trained as a mathematician, physicist or biologist.

What I am, is a pretty good problem solver who is able to work with very little information. So, although I have an 'intuitive feel' for non-linear dynamics, I'm afraid that I do not have the technical knowledge to assess your ideas. In fact, I was rather hoping to be able to gain insight into these phenomena from your good self.

I recieve emails from people who are far more informed about solitons than I. Invariably, I find myself at a disadvantage.

Of course, I am very interested in the work that you are doing and I wish to offer encouragemenet (if not practical help).

As for helping you with the transaltion of a text - well, perhaps I can try. It might even help me to undertstand these non-linear dynamics to a better degree. I cannot promise anything - please bear in mind that I am attempting to do a PhD. I would certainly like to gain a better undertstanding of your ideas, though.

I am very pleased and proud to be able to tell you all that my article will be published in a Springer volume - 'The Emerging Physics of Consciousness'. It's part of the Frontier series. Actaully I am also very nervous. If the ideas catch on then I might well find myself 'on the spot' and people will expect much more of me than I feel able to provide - at present.

These are exciting times and it is great to find myself amongst people who are inspired by the new ideas emerging in neuroscience.

Chris Davia

PS - Dianne - I have not forgotten that I promised you some more of my writings - I will get on to it soon. Thank's again.

PPS - Do any of your members have a working knowledge of Bose-Einstein condensates - Frohlic effect...etc????

[bernard]

Welcome on SomaSimple Forums, Chris,

I think that we are all pleased that you have had some time finally to join. :shade:

I'm not a physicist (made only one year at Uni), too. I have a wide but minimal culture about many subjects, unlike you (You have more than I). But we have, in common, a sense of synthesis and understanding that a piece is sometimes out of the scene...

I planned to do a visual basic training about my researches. Some more movies to come that show how Nature works at the molecular level, and thus at the miscroscopic level, and then...

About Bose-Einstein and so on, Im' afraid that it is very far from my knowledge but you may ask on this site (as I did). They are a bit direct in their replies but you have only to be precise with your askings.

Physics Forums (http://www.physicsforums.com/)

ps: I'm logged on this site with a somasimple username.
Gook luck with the paper!!! :thumbs_up:thumbs_up:thumbs_up

[bernard]

Hi SomaSimplers,

I found a book on this site

http://www.advancedphysics.org/forum/showthread.php?t=2149

Revolution in the Physiology of the Living Cell (http://www.amazon.com/gp/product/0894643983/qid=1133888116/sr=8-1/ref=sr_8_xs_ap_i1_xgl14/104-8093726-3675939?n=507846&s=books&v=glance)

I found similar points of view between my view about membranes and ions.
I'm trying to read this book but it seems a bit difficult.

I'll try to contact Gilbert N. LING.

[bernard]

J Neurosci Methods. (javascript:AL_get(this, 'jour', 'J Neurosci Methods.');) 2000 Nov 30;103(2):145-9. Related Articles, (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=11084206) Links (javascript:PopUpMenu2_Set(Menu11084206);) http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--linkinghub.elsevier.com-ihub-images-PubMedLink.gif (http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3048&uid=11084206&db=pubmed&url=http://linkinghub.elsevier.com/retrieve/pii/S0165027000003083)
The cost of an action potential.

Aiello GL (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Aiello+GL%22%5BAuthor%5D), Bach-y-Rita P (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Bach%2Dy%2DRita+P%22%5BAuthor%5D).

Dipartimento di Scienze Fisiche ed Astronomiche, Universita' di Palermo, Via Archirafi 36, 90123, Palermo, Italy. aiello@fisica.unipa.it

Neuronal modules, or 'cell-assemblies', comprising millions of mutually interconnected cells have been postulated to form the basis of many functions of the brain, such as mood, sleep, hunger, vigilance, and more. Depending on the extent of the module, neurocommunication in cell-assemblies might exceed metabolic resources. A medium-size (10000 neurons) module would require at least 10 J per l of brain, based on a calculated cost of an isolated action potential (AP) of 10(11)-10(12) molecules of ATP per cm(2) of cell membrane, with an absolute minimum of 10(6) ATP at a node of Ranvier. The figure matches the cost of depolarizing the unmyelinated axon of the large monopolar cell in the blowfly retina. A circuit model of the cell membrane, based on abrupt changes of Na(+) and K(+) conductances, is used to emulate the AP and to assess the resulting ionic unbalance. The cost of an AP is equated to the metabolic energy necessary to fuel ATP-based pumps that restore intracellular K(+). The high metabolic demand of a cell-assembly suggests that less expensive means of neurocommunication may be involved, such as non-synaptic diffusion neurotransmission (NDN), which would comply with a proposed law of conservation of space and energy in the brain.

PMID: 11084206 [PubMed - indexed for MEDLINE]

[bernard]

Ian provided this link on NOI group.

Fundamentals (NOI) (http://www.somasimple.com/forums/showthread.php?t=2234)

and in this one =>
How Nerve Cells Work Part I: (http://www.cerebromente.org.br/n09/fundamentos/transmissao/voo_i.htm)

we see :
Ions, Water and Membranes (http://www.cerebromente.org.br/n09/fundamentos/transmissao/salt_i.htm)- Diffusion and Membranes (http://www.cerebromente.org.br/n09/fundamentos/transmissao/difusao_i.htm)- Electrical Charge (http://www.cerebromente.org.br/n09/fundamentos/transmissao/electrical_i.htm)

Small pores in the surface of the permeable membrane allow the selective passage of ions. There are specific channels for each ion (sodium, chloride, potassium, etc.). The rate of passage is regulated by the number and size of pores. After a while, the concentration of both ions (green and yellow bars) will be the same on both sides of the membrane.

Contributing to the membrane polarity, all potassium ions that come out of the cell form a fine positive layer on the outside, just by the membrane.

Things would stay the same in perpetual equilibrium except for two things: the sudden changes of action potentials (which inverts polarity for a brief one or two microseconds before the sodium-potassium pump arranges things nicely up again), and the continuous input of metabolic energy to the pump.

One interesting thing is that the quantity of ions which is required to pass from one side to the other in order to produce a potential difference is exceedingly small.

[bernard]

Here comes a view that is similar to mine.
: Biophys J. (javascript:AL_get(this, 'jour', 'Biophys J.');) 2003 Nov;85(5):2854-64. Related Articles, (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=14581190) Links (javascript:PopUpMenu2_Set(Menu14581190);) http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--highwire.stanford.edu-icons-externalservices-pubmed-free-biophysj-free.gif (http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3051&uid=14581190&db=pubmed&url=http://www.biophysj.org/cgi/pmidlookup?view=long&pmid=14581190) http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--www.ncbi.nlm.nih.gov-corehtml-query-pubmed-pmc.gif (http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3494&uid=14581190&db=pubmed&url=http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=14581190)
Electrostatic model of S4 motion in voltage-gated ion channels.

Lecar H (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Lecar+H%22%5BAuthor%5D), Larsson HP (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Larsson+HP%22%5BAuthor%5D), Grabe M (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Grabe+M%22%5BAuthor%5D).

Department of Molecular and Cell Biology, University of California at Berkeley, Berkeley, California 94720, USA. hlecar@uclink4.berkley.edu

The S4 transmembrane domain of the family of voltage-gated ion channels is generally thought to be the voltage sensor, whose translocation by an applied electric field produces the gating current. Experiments on hSkMI Na(+) channels and both Shaker and EAG K(+) channels indicate which S4 residues cross the membrane-solution interface during activation gating. Using this structural information, we derive the steady-state properties of gating-charge transfer for wild-type and mutant Shaker K(+) channels. Assuming that the energetics of gating is dominated by electrostatic forces between S4 charges and countercharges on neighboring transmembrane domains, we calculate the total energy as a function of transmembrane displacement and twist of the S4 domain. The resulting electrostatic energy surface exhibits a series of deep energy minima, corresponding to the transition states of the gating process. The steady-state gating-charge distribution is then given by a Boltzmann distribution among the transition states. The resulting gating-charge distributions are compared to experimental results on wild-type and charge-neutralized mutants of the Shaker K(+) channel.

Publication Types:
Evaluation Studies (javascript:AL_get(this, 'ptyp', 'Evaluation Studies');)
Validation Studies (javascript:AL_get(this, 'ptyp', 'Validation Studies');)
PMID: 14581190 [PubMed - indexed for MEDLINE]

[bernard]

J Physiol. (javascript:AL_get(this, 'jour', 'J Physiol.');) 1994 Sep 1;479 ( Pt 2):183-97. Related Articles, (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Display&dopt=pubmed_pubmed&from_uid=7799220) Links (javascript:PopUpMenu2_Set(Menu7799220);) http://www.ncbi.nlm.nih.gov/entrez/query/egifs/http:--www.ncbi.nlm.nih.gov-corehtml-query-pubmed-pmc.gif (http://www.ncbi.nlm.nih.gov/entrez/utils/lofref.fcgi?PrId=3494&uid=7799220&db=pubmed&url=http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=7799220)
Na(+)-activated K+ channels localized in the nodal region of myelinated axons of Xenopus.

Koh DS (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Koh+DS%22%5BAuthor%5D), Jonas P (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Jonas+P%22%5BAuthor%5D), Vogel W (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Vogel+W%22%5BAuthor%5D).

Physiologisches Institut, Justus-Liebig-Universitat, Giessen, Germany.

1. A potassium channel activated by internal Na+ ions (K+Na channel) was identified in peripheral myelinated axons of Xenopus laevis using the cell-attached and excised configurations of the patch clamp technique. 2. The single-channel conductance for the main open state was 88 pS with [K+]o = 105 mM and pS with [K+]o = 2.5 mM ([K+]i = 105 mM). The channel was selectively permeable to K+ over Na+ ions. A characteristic feature of the K+Na channel was the frequent occurrence of subconductance states. 3. The open probability of the channel was strongly dependent on the concentration of Na+ ions at the inner side of the membrane. The half-maximal activating Na+ concentration and the Hill coefficient were 33 mM and 2.9, respectively. The open probability of the channel showed only weak potential dependence. 4. The K+Na channel was relatively insensitive to external tetraethylammonium (TEA+) in comparison with voltage-dependent axonal K+ channels; the half-maximal inhibitory concentration (IC50) was 21.3 mM (at -90 mV). In contrast, the channel was blocked by low concentrations of external Ba2+ and Cs+ ions, with IC50 values of 0.7 and 1.1 mM, respectively (at -90 mV). The block by Ba2+ and Cs+ was more pronounced at negative than at positive membrane potentials. 5. A comparison of the number of K+Na channels in nodal and paranodal patches from the same axon revealed that the channel density was about 10-fold higher at the node of Ranvier than at the paranode. Moreover, a correlation between the number of K+Na channels and voltage-dependent Na+ channels in the same patches was found, suggesting co-localization of both channel types. 6. As weakly potential-dependent ('leakage') channels, axonal K+Na channels may be involved in setting the resting potential of vertebrate axons. Simulations of Na+ ion diffusion suggest two possible mechanisms of activation of K+Na channels: the local increase of Na+ concentration in a cluster of Na+ channels during a single action potential or the accumulation in the intracellular axonal compartment during a train of action potentials.

PMID: 7799220 [PubMed - indexed for MEDLINE]

[BB]

Bernard,
How is your paper and theory progressing?
Cory

[bernard]

Hi Cory,

Thanks for the interest reguarding my passionate madness.

The original paper needs a huge refinenement. I'm actually collecting clues showing that the actual theory holds failures.

I'll bring some animations that clearly shows how and why the alternative solution is more effective and "natural".

I'm asking some biologists with "innocent" questions and I'm amazed with the collected responses => Some refuse to continue the discussion and others recite their lessons without no doubt.

The main problem with the "original" theory is missing links between very important behaviours in the axon. The transmission is explained by the myelinated axon and thus the theory is extended to the nonmyelinated one.

But evolution says clearly that low speed fibres were born before these latests.

Here is an example of a missing link in the reasonning coming from this page: http://en.wikipedia.org/wiki/Action_potential

The action potential

When a stimulus arrives at a receptor or nerve ending, its energy causes a temporary reversal of the charges on the neuron cell surface membrane. As a result, the negative charge of 70mV inside the membrane becomes a positive charge of around +40mV. This is known as the action potential, and in this condition the membrane is said to be depolarised. (See depolarization (http://en.wikipedia.org/wiki/Depolarization)) This depolarization occurs because channels in the axon membrane change shape, and hence open or close, depending on the voltage across the membrane. They are therefore called voltage-gated ion channels (http://en.wikipedia.org/wiki/Voltage-gated_ion_channel). The sequence of events is described below.
At resting potential some potassium voltage-gated channels are open but the sodium voltage-gated channels are closed.
The energy of the stimulus causes the sodium voltage-gated channels in the neuron cell surface membrane to open and therefore sodium ions diffuse in through the channels along their electrochemical gradient. Being positively charged, they begin a reversal in the potential difference across the membrane.
As sodium ions enter, so more sodium channels open, causing an even greater influx of sodium ions. This is an example of positive feedback.
Once the action potential of around +40mV has been established, the voltage gates of the sodium channels, sensitive to the now positive surroundings, close (so further influx of sodium is prevented). While this occurs, the voltage gates on the potassium channels begin to open.
With some potassium voltage-gated channels now open, the electrical gradient that was preventing further outward movement of potassium ions is now reversed, causing more potassium channels to open. This means that yet more potassium ions diffuse out, causing repolarisation of the neuron.
The outward movement of these potassium ions causes the temporary overshoot of the electrical gradient, with the inside of the neuron being more negative (relative to the outside) than usual. This is called hyperpolarisation (hyperpolarization (http://en.wikipedia.org/wiki/Hyperpolarization)). The gates on the potassium channels now close and the activities of the sodium-potassium pumps cause sodium ions to be pumped out and potassium ions in, once again. The resting potential of -70mV is re-established and the neuron is said to be repolarised.
and a bit later in the text =>

Speed of propagation

Action potentials propagate faster in axons of larger diameter, other things being equal. They typically travel from 10-100 m/s. The main reason is that the axial resistance of the axon lumen is lower with larger diameters, because of an increase in the ratio of cross-sectional area to membrane surface area. As the membrane surface area is the chief factor impeding action potential propagation in an unmyelinated axon, increasing this ratio is a particularly effective way of increasing conduction speed.
and,

Detailed mechanism The main impediment to conduction speed in unmyelinated axons is membrane capacitance (http://en.wikipedia.org/wiki/Capacitance). In an electric circuit (http://en.wikipedia.org/wiki/Electric_circuit), the capacity of a capacitor (http://en.wikipedia.org/wiki/Capacitor) can be decreased by decreasing the cross-sectional area of its plates, or by increasing the distance between plates.
Please find the capacitance in the first five points explanation. :embarasse

[bernard]

And if you look closely to the capacitor =>

http://en.wikipedia.org/wiki/Capacitor

You'll see that energy exists between plates and communication is oriented them inexorably. If membrane acts as a capacitor which has a capacitance then the electric flow is only vertical. There is no way to create a lateral motion as we are seeing it in axons. The wave is going and capacitors haven't such a property.

[BB]

Hi Bernard,
Glad to hear that you are continuing to refine and pursue. I wish that I understood the intricate mechanics better and could engage in discussion better on your theory.

On capacitance, I know that I was taught about electrical impluses traveling the membrane. And ranvier nodes (I think that's what the spaces between the myelin are called?) allow for a bit of skipping over for parts of the membrane.

Could you clarify this quote for me?

The transmission is explained by the myelinated axon and thus the theory is extended to the nonmyelinated one.


Are you saying the the existing theory makes sense for myelinated axons, but not nonmyelinated?

Cory

[bernard]

Cory,

The actual theory doesn't make sense in both scenario.
The five points cited are perfectly clear and may explain the lateral motion but it doesn't (seems) work for myelinated axons. So they created a theory which explains the saltatory conduction and said it worked also for non myelinated. But doing so has a price, they reject the five points since it does not need a capacitance.

And if it doesn't need a capacitance it discards also its use with myelinated axons. That is the problem. The capacitance is mandatory in their explanations for myelinated axons.

They created a circular reference in the theory. An endless loop that is useless. They cite a theory they do not use in non myelinated conduction as the explained process/solution for myelinated.

[bernard]

Hi All,

Reading the old writings I made let me think that a refinement is not only possible but really necessary.

The works of Professor I TASAKI complete my "vision" about a more subtle theory. It is of course, more complex but so natural and understandable.

Nature had no choice! We tried to glue some simple thoughts and simple theories on a complex interactive set of properties and constraints.

They become preponderant in ralation of the size of the axons.

In a small diameter, the electrostatic behaviour is strong as the elasticity of membrane. Ions have "problems" to come in and ions channels are distant because their repelling forces. slow because the resultant force is largely used to "win" the membrane.
Membrane, with phase transitions, plays a major role because it acts as a lock and favors an unidirectional travel of the AP.
Increasing diameter, give more electrostaic/volumic forces and a good compromise. In larger versions, the membrane is too weak and too deformable and the speed is thus limited as it is comfirmed. Nature, with myelinated axons, tried to tighten the membrane to give some "boost" like in small fibres. But, the adopted solution is better => a dual set of forces electostatic/volume that send a pressure wave in a tight tube. Bravo, simple and marvelously efficient.