Propagation of Action Potential

[bernard]

Hello SomaSimplers,



This page comes from the Molecular cell ebook:
http://www.ncbi.nlm.nih.gov/books/bv...c4.figgrp.2043

the picture comes from this chapter =>
http://www.ncbi.nlm.nih.gov/books/bv...4.section.2027

Of course, I do not think that it's a possible mechanism. It doesn't work but I have to show you, how, why and where!

[bernard]

The text below is brought from the cited page and shows that it exists 2 currents flows: an active (ions crossing the membranes via ions channels and a passive one, induced by cable property)

Myelination Increases the Speed and Efficiency of Action Potential Propagation in Nerve Cells
The axons of many vertebrate neurons are insulated by a myelin sheath, which greatly increases the rate at which an axon can conduct an action potential. The importance of myelination is dramatically demonstrated by the demyelinating disease multiple sclerosis, in which myelin sheaths in some regions of the central nervous system are destroyed; where this happens, the propagation of nerve impulses is greatly slowed, often with devastating neurological consequences.

Myelin is formed by specialized supporting cells called glial cells. Schwann cells myelinate axons in peripheral nerves and oligodendrocytes do so in the central nervous system. These glial cells wrap layer upon layer of their own plasma membrane in a tight spiral around the axon (Figure 11-30), thereby insulating the axonal membrane so that little current can leak across it. The myelin sheath is interrupted at regularly spaced nodes of Ranvier, where almost all the Na+ channels in the axon are concentrated. Because the ensheathed portions of the axonal membrane have excellent cable properties (in other words, they behave electrically much like well-designed underwater telegraph cables), a depolarization of the membrane at one node almost immediately spreads passively to the next node. Thus, an action potential propagates along a myelinated axon by jumping from node to node, a process called saltatory conduction. This type of conduction has two main advantages: action potentials travel faster, and metabolic energy is conserved because the active excitation is confined to the small regions of axonal plasma membrane at nodes of Ranvier

[Diane]

I think that glia, arising as they do from neural crest which is originally nerve cell, would be a very important secondary system, passing info along cell to cell through gap junctions, neurochemically. They do that in the brain as I recall, do you think they can do that across nodes out in the periphery? (Wouldn't it be interesting if it was determined that myalin has a signalling system? )

[bernard]

Diane,

Your point of view makes sense and tell us that glia/myelin cells were forgotten in the riddle. This is a living point of view. :thumbs_up

I was thinking about more simple things. :embarasse

I'll try to bring facts and offer the Occam chainsaw 101 for your choice?

BTW, I use the Occam chainsaw but knew a razor? :embarasse

[bernard]

Perhaps the best proof available actually against the "cable theory".


J Cell Biol. 2005 May 9;169(3):527-38. Related Articles, Links
Tight junctions in Schwann cells of peripheral myelinated axons: a lesson from claudin-19-deficient mice.

Miyamoto T, Morita K, Takemoto D, Takeuchi K, Kitano Y, Miyakawa T, Nakayama K, Okamura Y, Sasaki H, Miyachi Y, Furuse M, Tsukita S.

Department of Cell Biology, Graduate School of Medicine, Kyoto University, Japan.

Tight junction (TJ)-like structures have been reported in Schwann cells, but their molecular composition and physiological function remain elusive. We found that claudin-19, a novel member of the claudin family (TJ adhesion molecules in epithelia), constituted these structures. Claudin-19-deficient mice were generated, and they exhibited behavioral abnormalities that could be attributed to peripheral nervous system deficits. Electrophysiological analyses showed that the claudin-19 deficiency affected the nerve conduction of peripheral myelinated fibers. Interestingly, the overall morphology of Schwann cells lacking claudin-19 expression appeared to be normal not only in the internodal region but also at the node of Ranvier, except that TJs completely disappeared, at least from the outer/inner mesaxons. These findings have indicated that, similar to epithelial cells, Schwann cells also bear claudin-based TJs, and they have also suggested that these TJs are not involved in the polarized morphogenesis but are involved in the electrophysiological "sealing" function of Schwann cells.

PMID: 15883201 [PubMed - indexed for MEDLINE]


Here is the pdf file =>
www.somasimple.com/pdf_files/tight_junctions.pdf

[bernard]

Hi All,

The most important pieces of the previous paper are below.

[bernard]

I'll add this lovely old piece (I'll give the author later).
It explains what is the saltatory conduction and precisely the two phases its exists (?) during the process.

We musn't forget that a myelinated neuron begins its life without myelin. It acts in its early life as an unmyelinated one.

[Diane]

Besides, in the ganglion, myelin becomes completely irrelevant; it's an orgy of intercommunication in there, according to Grieve's (see post #18).

[bernard]

Absolutely Diane,

Myelin enhances only the speed of communication.
I just wanted to point out the origin of electrical behaviour in axons. The paper was written in 1950 but remains (for me) the trigger of misunderstandings about this perfect thing that is neuron.

The previous attachments are saying that removing tight junctions (a physical proterty = tightness) from axons creates loose myelin which gives delayed action potentials. If meylin was really an electrical insulator, removing tight junctions will have no effect.

So the electrical theory fails, once again, to fit the fact.

[bernard]

I think that you'll like this one, Diane? It fits your "tunneling" theory.
Unmyelinated fibres have a physical travelling wave during APs.
Good news for fluid things!


Biophys J. 1990 Mar;57(3):633-5. Related Articles, Links
Volume expansion of nonmyelinated nerve fibers during impulse conduction.

Tasaki I, Byrne PM.

Unit on Neurobiology, National Institute of Mental Health, Bethesda, Maryland 20892.

Nonmyelinated nerve fibers undergo rapid volume expansion while carrying an impulse. This volume expansion is incurred as a consequence of a lateral expansion of the excited portion of the fibers, where the superficial layer is transformed into a low-density structure.

PMID: 2306506 [PubMed - indexed for MEDLINE]

[Diane]

Interesting.. like a bolus through a python. Biomechanics of neurons?

[bernard]

Or like a limb of an amoeba. Nature uses and reuses the same useful tips. Just with changed scales.

Neuron is a mobile cell.

[Diane]

At least that growth cone sure is.. like a pitbull on a leash who smells raw steak...

[bernard]

[flash]http://www.somasimple.com/flash_anims/ap_001.swf[/flash]


action potential 001

[Diane]

Non-myelinated nerve fibres undergo rapid expansion... makes me see a picture in my head of a bulge moving down a garden hose, bolus in a python, etc. Is the myelin there to "contain" bulges, smooth them out? Make it harder for them to "bulge"? Does "bulge transport" move faster in a stiffer pipe than it does in a flexible one? It makes sense on first take, just that physically surrounding a tube would change the deformability of that tube..however..

About myelin being an active communicator rather than a buttress, and definitely instead of it being a "nurse cell", I found a clue in one of Kevin McHenry's latest essays:
He discusses white blood cellls and their role in inflammation, then adds this:

Last of all we come to the glia, which surround neurons, which used to be called "supportive cells" by Dr. Frankensteins who had no idea what glia actually were doing there. We now know that glia perform no structural role whatsoever and therefore cannot be "supportive". The latest word is that these cells are involved in inflammation, neuroinflammation to be specific. They spit out materials too, such as growth factors, which cause the genes of pain neurons to go postal (hog wild) and take over the protein factories in the genes which make acids.

Eeeeeeeyew. That would be why axons get AIGS's. For the longest time I had in my head the idea that glia and Schwann's buffered the axons, kept them "clothed", kept them "insulated".. (to be fair, McHenry is not talking peripherally, only centrally. Maybe Schwann's are functionally distinct from glia somehow...)

Sorry, off track now. Back to axon bulges Bernard.