The first excellent query raised by somasimple in this thread is: what is an appropriate model in which to understand Huxley and Stämpfli's records of the fast but finite AP propagation speed in the internode of a myelinated axon?
Huxley and Stämpfli themselves describe nodes as "active" and internodes as "passive". A naive application of linear passive cable theory gives an infinite speed of propagation for the minimal disturbance, and does not allow traveling wave solutions from which a signal velocity may be easily defined. This does not necessarily mean that a signal velocity cannot be defined, only that we may have to be careful about it. We should, however, ask whether Huxley and Stämpfli and cable theory use "passive" in the same sense. The HS model of myelinated axons appears to be a modification of the HH model for unmyelinated axons, and may therefore be relevant. In fact, a similar question about the meaning of "active" and "passive" can be asked about unmyelinated axons, as somasimple previously indicated.
The quotes in blue are somasimple's queries from an earlier thread:
https://www.physicsforums.com/showthread.php?t=254044.
The Action Potential propagation involves a passive event called: Passive Spread or Electrotonic conduction.
Here is some references:
[NB: I have edited the quote by numbering the references - atyy]
R1 http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mcb.figgrp.6138
R2 http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=.0zyfzkapx787Lxyk2TNcPpbCOnVmwIAZMxK6R2
R3 http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mcb.figgrp.6145
R4 http://butler.cc.tut.fi/~malmivuo/bem/bembook/03/03.htm
It is defined a Constant Length that enables this passive event.
I brought these examples because they are the rare that have temporal values.
http://hawk.med.uottawa.ca/public/re...pagationAP.pdf
http://www.ncbi.nlm.nih.gov/books/bv...cb.figgrp.6145
This one says that the AP (of 2 ms duration) travels/runs at 1 mm/ms. So it must be a thin fiber since it runs at 1m/s. The space constant of such a fiber is around 0.1/0.2 mm but the "length" of the AP is 2mm. Centered on the peak value of the AP, the space constant is too short to activate any next patch of membrane.
I consider the queries excellent because R1 and R2 use the term "passive" in describing AP propagation, but as stated in post #29 of this thread:
So in fact, the linear passive cable equation is NOT the standard model for AP propagation in unmyelinated axons and somasimple is absolutely correct on that point!
Furthermore, R4, a discussion of linear passive cable theory for neurons, is a chapter entitled "subthreshold membrane phenomena", and therefore explicitly excludes APs. The reason AP length can be greater than the passive space constant is that the HH model includes passive and active elements, with no purely passive patch in the unmyelinated axon. R2 indicates this schematically with active Na
+ channels distributed continuously along the entire axon length.
Now, if the HH model for unmyelinated axons contains both passive and active elements, then it presumably faces the same problem that the minimal disturbance propagates in a passive circuit with infinite velocity. Yet the HH model derives, in conjunction with the active elements, a traveling wave equation with well-defined finite signal propagation velocity. This may be relevant to understanding the HS model, since it is a modification of the HH model. R4 links to the following chapter which discusses the integration of passive and active elements in the HH model:
http://butler.cc.tut.fi/~malmivuo/bem/bembook/04/04.htm
A second excellent query raised by somasimple in this thread concerns the birectionality of the passive elements, whereas AP travel is unidirectional. R3 suggests that this may again be resolved by considering the integration of passive and active elements:
http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mcb.figgrp.6145
Finally, I note that somasimple's queries are not arcane, but pertain to multiple sclerosis, a disease of myelination.