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It seems that the following quote from the article is wrong.
The speed of the signal from one node to another is the speed of the induced electromagnetic wave, that is, the speed of light in interaction with transparent materials like the cytoplasm (~100.000.000 metres per second).
I'm quoting from "Textbook of Medical Physiology", 11ed, by Guyton and Hall, page 68:
The velocity of conduction in nerve fibers varies from as little as 0.25 m/sec in very small unmyelinated fibers to as great as 100 m/sec (the length of a football field in 1 second) in very large myelinated fibers.
Furthermore, on the same page there is an illustration that shows the flow of electrical current in the axoplasm of a myelinated axon. Clearly, electrical current in the axoplasm does not have the speed of light because it is affected by drifting ions.
--
82.81.69.96 (
talk) 17:28, 14 April 2009 (UTC)
I added a diagram of the structure of the neuron to make this page a bit more understandable without reading other articles.
Ideally, someone would make an animation like this: http://www.brainviews.com/abFiles/AniSalt.htm or this: http://www.edumedia-sciences.com/en/a503-saltatory-conduction or this: http://faculty.stcc.edu/AandP/AP/AP1pages/nervssys/unit11/saltator.htm
with an open license.
-- Bcjordan ( talk) 16:58, 12 September 2009 (UTC)
Relative to the mechanism of saltatory conduction, would it be accurate to say that electrotonic conduction is involved in causing a voltage at one node to affect the next node, and thus that saltatory conduction is a combination of the action potential and electrotonic conduction? 75.6.227.116 ( talk) 08:47, 27 March 2011 (UTC)
I've tried to rewrite the section in order to clear this up. Is it clearer now? -- Tryptofish ( talk) 21:52, 7 October 2011 (UTC)
This article is incorrect. It states "Myelinated axons only allow action potentials to occur at the unmyelinated nodes of Ranvier that occur between the myelinated internodes". The action potential is the depolarization of the membrane due to the axial flow of positive charges. This does *NOT* jump from node to node. It travels down the whole length of the axon (both nodes and internodes). The difference is that at within the internode (myelinated segment) the action potential propagates passively. That means that positive charges are simply diffusing - they are not exiting or entering the cell. When the action potential reaches a node, dense clusters of voltage gated sodium channels are triggered to regenerate the action potential by opening and allowing inward flow of positive Na+ ions. This is called the "transmembrane current" and THIS is what "jumps" from node to node. This is also the time-consuming step of the action potential. The reason why myelin increases action potential conduction velocity is because it decreases the amount of transmembrane current. In unmyelinated axons, the transmembrane current occurs during the entire length of the axon. Transmembrane current is needed to regenerate the action potential, but it turns out you don't need the ENTIRE axon to have transmembrane current in order to maintain an axon potential. The myelin optimizes the amount of transmembrane current so it is enough to regenerate action potential but not too much so it's not "wasting" time and energy regenerating it when it would be faster to just let the positive charges diffuse some distance passively until the next regeneration site (node). Hope I've made that clear.
In fact signals are not conducted inside neurons but propagated through and across the membrane, in this case, in the spaces in between the "sausage links." The conduction of electricity approaches light speeds but the propagation of charges along an axon is extremely slow by comparison. When I studied physiological psychology, I never heard anything referred to as conduction. I will do some more research. Mea ( talk) 01:06, 6 May 2014 (UTC)
Is the primary mode of reaching resting membrane potential following hyperpolarization not the activity of inward rectifier potassium channels? It appears that the intent of the statement in the article is to indicate that the decreased non-insulated surface area (of ion channel-rich membrane) decreases the amount of energy dependent active transport for maintenance of constitutive resting potential (ie independent of action potential). Perhaps this section could be rephrased to disambiguate the statement. — Preceding unsigned comment added by 66.243.219.231 ( talk) 22:20, 7 December 2016 (UTC)
Transmission lines can contain parallel conductance and capacitance increasing signal propagation velocity and decreasing intensity. The ion channels providing parallel conductance could require editing or elaboration to the quotes "...Regenerating the action potential...", "...Thus refreshing the signal" and "...without any degradation of the signal..."
This article is rated Start-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | ||||||||||||||||||||||||
|
It is requested that an anatomical diagram or diagrams be
included in this article to
improve its quality. Specific illustrations, plots or diagrams can be requested at the
Graphic Lab. For more information, refer to discussion on this page and/or the listing at Wikipedia:Requested images. |
It seems that the following quote from the article is wrong.
The speed of the signal from one node to another is the speed of the induced electromagnetic wave, that is, the speed of light in interaction with transparent materials like the cytoplasm (~100.000.000 metres per second).
I'm quoting from "Textbook of Medical Physiology", 11ed, by Guyton and Hall, page 68:
The velocity of conduction in nerve fibers varies from as little as 0.25 m/sec in very small unmyelinated fibers to as great as 100 m/sec (the length of a football field in 1 second) in very large myelinated fibers.
Furthermore, on the same page there is an illustration that shows the flow of electrical current in the axoplasm of a myelinated axon. Clearly, electrical current in the axoplasm does not have the speed of light because it is affected by drifting ions.
--
82.81.69.96 (
talk) 17:28, 14 April 2009 (UTC)
I added a diagram of the structure of the neuron to make this page a bit more understandable without reading other articles.
Ideally, someone would make an animation like this: http://www.brainviews.com/abFiles/AniSalt.htm or this: http://www.edumedia-sciences.com/en/a503-saltatory-conduction or this: http://faculty.stcc.edu/AandP/AP/AP1pages/nervssys/unit11/saltator.htm
with an open license.
-- Bcjordan ( talk) 16:58, 12 September 2009 (UTC)
Relative to the mechanism of saltatory conduction, would it be accurate to say that electrotonic conduction is involved in causing a voltage at one node to affect the next node, and thus that saltatory conduction is a combination of the action potential and electrotonic conduction? 75.6.227.116 ( talk) 08:47, 27 March 2011 (UTC)
I've tried to rewrite the section in order to clear this up. Is it clearer now? -- Tryptofish ( talk) 21:52, 7 October 2011 (UTC)
This article is incorrect. It states "Myelinated axons only allow action potentials to occur at the unmyelinated nodes of Ranvier that occur between the myelinated internodes". The action potential is the depolarization of the membrane due to the axial flow of positive charges. This does *NOT* jump from node to node. It travels down the whole length of the axon (both nodes and internodes). The difference is that at within the internode (myelinated segment) the action potential propagates passively. That means that positive charges are simply diffusing - they are not exiting or entering the cell. When the action potential reaches a node, dense clusters of voltage gated sodium channels are triggered to regenerate the action potential by opening and allowing inward flow of positive Na+ ions. This is called the "transmembrane current" and THIS is what "jumps" from node to node. This is also the time-consuming step of the action potential. The reason why myelin increases action potential conduction velocity is because it decreases the amount of transmembrane current. In unmyelinated axons, the transmembrane current occurs during the entire length of the axon. Transmembrane current is needed to regenerate the action potential, but it turns out you don't need the ENTIRE axon to have transmembrane current in order to maintain an axon potential. The myelin optimizes the amount of transmembrane current so it is enough to regenerate action potential but not too much so it's not "wasting" time and energy regenerating it when it would be faster to just let the positive charges diffuse some distance passively until the next regeneration site (node). Hope I've made that clear.
In fact signals are not conducted inside neurons but propagated through and across the membrane, in this case, in the spaces in between the "sausage links." The conduction of electricity approaches light speeds but the propagation of charges along an axon is extremely slow by comparison. When I studied physiological psychology, I never heard anything referred to as conduction. I will do some more research. Mea ( talk) 01:06, 6 May 2014 (UTC)
Is the primary mode of reaching resting membrane potential following hyperpolarization not the activity of inward rectifier potassium channels? It appears that the intent of the statement in the article is to indicate that the decreased non-insulated surface area (of ion channel-rich membrane) decreases the amount of energy dependent active transport for maintenance of constitutive resting potential (ie independent of action potential). Perhaps this section could be rephrased to disambiguate the statement. — Preceding unsigned comment added by 66.243.219.231 ( talk) 22:20, 7 December 2016 (UTC)
Transmission lines can contain parallel conductance and capacitance increasing signal propagation velocity and decreasing intensity. The ion channels providing parallel conductance could require editing or elaboration to the quotes "...Regenerating the action potential...", "...Thus refreshing the signal" and "...without any degradation of the signal..."