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"An action potential is an electrical pulse that changes the voltage (potential) across a cell membrane. In muscle and nerve cells, this rapid change in voltage leads to an action such as muscular contraction or neurotransmitter release. These actions are usually a consequence of calcium ions entering the cell during the rapid change in voltage. "
I think any definition has to include the idea of propagation, if not the idea of a wave, which is the mode of propagation in the first kind of action potential most people think of, which is in nerves. It's just wrong that calcium "usually" causes an AP. According to the Hodgkin-Huxley theory, based on the way things work in the giant axon of the squid, all you need are sodium channels and potassium channels. Calcium is important in coupling excitation (the AP) to contraction in muscle, but at the neuromuscular junction its acetylcholine receptors that initiate the action potential, and these will predominantly be carrying sodium into the cell. I suspect they don't permit calcium at all.
Maybe I'm being pedantic here, but if you look at the phrase "action potential", it is clearly a noun. It should refer to the level of potential necessary to incite action (or some similar aspect of the amount of potential), not the process of changing potential. Is all of neurochemistry suffering a semantic deficit, or just this article? p.s. I'm coming from an electronics background, where potential clearly means "voltage" -- which, in this case, it literally does, so I think I'm standing on solid semantic ground. 12.210.113.235 14:20, 1 June 2006 (UTC)
What does the cartoon of the phospholipid membrane have to do with an action potential? There aren't even any ion channels in the drawing, as far as I could tell. Could someone find a nice graph of an action potential (i.e. a voltage-time graph showing membrane potential increasing to threshold, then firing, then a refractory period)? Sayeth 19:52, Jul 29, 2004 (UTC)
I agree the top picture should be a voltage-time graph. Perhaps when one is found the membrane image could move further down the article? Richard Taylor
Thanks for the new caption, Richard. It makes the drawing much more relevant, but I agree that there's still some improvement possible with a second picture. Sayeth 19:52, Jul 29, 2004 (UTC)
I had a few minutes of spare time and decided to redraw Chris' image in Adobe Illustrator. It's basically the same image with some antialiasing and smaller font sizes for readability. Would anyone object if I replaced the current image with my version? -- Diberri | Talk 17:22, Jul 30, 2004 (UTC)
Is the refractory period a) that long and b) is the hyperpolarisation so "hyper" (ie does it go so negative?). I thougth that both were smaller. Batmanand 14:16, 22 Jun 2005 (UTC)
Hi this article no longer meets the criteria for a featured article because it does not cite its sources. Please help fix this so that all featured articles can meet the same standards. Best would be the most trusted resources in the field being added, some print resources especially, but also online references are better than none. Those sources would likely help with good material to further improve the article anyway. - Taxman 23:00, Oct 26, 2004 (UTC)
I'm familiar with the contents of Kandel, X and Schwartz. Yes, the content of that one aggrees with what is said here. I've not read Bear (although he did once hit on my girlfriend ;-), but this is all such "textbook stuff" that I'm sure Bear also supports what is in here.
I've also added references to the primary literature: the original HH papers and also an updated look at HH-models. Synaptidude 5 July 2005 20:58 (UTC)
The first paragraph reads:
What is the evidence that the speed of an action potential contrains the size of an organism or organ? It is not discussed in the article.
Also, there are propagating action potentials in plants. They can move along the phloem cell membranes similar to nerves. A good example of this is the sensitive mimosa plant. It's leaflets close in response to touch and the movement can be seen to propagate down the stem. This is due to motor cells sequentially releasing water due to the change in membrane potential as the action potential progress' down the stem. This was observed and published by Charles Darwin in his less famous book The power of movement in plants. John Murray, London, 1880. There are two big differences between plant and animal action potentials: 1) plant AP's are much slower; 2) plant AP's are generated with K+ and anions, unlike animals that use K+ and Na+ ions. David D. 15:32, 3 May 2005 (UTC)
You know, you could argue for days on end about chicken/egg aspects of evolutionary changes. I'm completely unfamiliar with any literature on action potentials and evolution, and yet it would seem obvious that the relationship between the two will be complex, probably showing causality in both directions (i.e. action potential propagation limits body size at the same time that body size limits axon diameter. Since evolutionary statements such as the one made in this article are often just informed speculation anyway, this whole problem can be (and has been) fixed by using the all-purpose scientist solution: "when you've got a feasible idea that you can't prove, say "may". Synaptidude 5 July 2005 21:05 (UTC)
I relabeled the graph showing the voltage-time relationships of the action potential. The former labels were slightly misleading in the following ways. 1) "Depolarization" and "Hyperpolarization" have been replaced with "Rising" and "Falling Phase". First, these are the correct terminologies in use by electrophysiologists. Second, the Rising Phase, once it crosses 0 mV is actually hyperpolarizing (see hyperpolarization. Likewise, the falling phase before it reaches 0 mV is actually depolarizing (see depolarization). This is why electrophysiologists don't use those terms to describe the rising and falling phases (each is a mixed hyper/depolarization). 2) The label "Refractory Period" has been replaced by "Undershoot". This is because the label incorrectly implied that the undershoot of membrane potental at the end of the action potential is the basis for the refractory period. The basis for the refractory period is actually a change in the action potential threshold caused by sodium channel inactivation (which has nothing directly to do with the undershoot). The undershoot is actually too large in this diagram, but I decided not to fix this at this time. According to the voltage scale used, the undershoot would go to approx. -100 mV. This is below Ek, and therefore physically impossible. 3)I've added ~ marks to the voltage scale of the y-axis. This is to indicate that the values of resting, threshold and peak potentials are approximate. For example, neurons rest anywhere from -80 to -55 mV. Thresholds and peaks vary similarly. 4) I've added a label for "overshoot", that is, the part of the action potential that overshoots 0 mV. Synaptidude 5 July 2005 18:59 (UTC)
Yes, thanks. I see that now. I guess it's time to do something about it. Synaptidude 5 July 2005 21:10 (UTC)
I'll have to check, but I think it was more likely Cole than H&H who "discovered" the propagating nature of action potentials. I think one could actually make a pretty strong argument for Sherington, who certainly knew that nerve impulses were propagated, although he didn't know specifically about action potentials per se
I suggest putting Part A and Part B of the first figure like this:
A
B
As it is now, it is leaving too little room for the main text along the left side of the page. -- Memenen 9 July 2005 16:52 (UTC)
simplicity ? -- AHands 21:39, 10 August 2005 (UTC)
Your childish vandalism of this article has been noted and reported to your ISP, as well as your parents. Synaptidude 23:48, 21 November 2005 (UTC)
Reading the suggestions in the featured review section, I have undertaken some changes (hope they are improvments)
1) I've re-written the introduction to make it more general and accurate. The accuracy part is the the "sets the pace of thought" statement. I have removed this because there is no evidence for this. Most current thought is that the pace of thought is set by the speed of neural osicillators that are made of networks of many neurons. While action potentials certainly subserve parts of the function of these oscillators, they are not the rate-limiting steps. It would be no more accurate to say that the frequencies coming from a radio speaker are set by the speed of electron travel through copper. Synaptidude 00:11, 22 November 2005 (UTC)
2) made some changes to clarify and more accurately reflect how the action potential is initiated
3) Added a section of "Why" the body uses action potentials
more to come Synaptidude 01:45, 22 November 2005 (UTC)
I flipped over to this Talk page to make some witty comment about how in depth this article is, and then I noticed it's a featured article...someone really knows their stuff heh
This was the version promoted in February of 2004, and
these are the changes made since. Article has been completely rewritten. The new version is quite a bit longer, and appears to be more comprehensive. The only significant issue I see is the diagram next to the lead, which makes for some very bad formatting (the lead is squeezed into really, really short lines), and the diagram seems a bit complex for the lead anyway (though I recognize this was likely done because no real image could be used for this article). Also, I don't like the section heading "Noteworthy characteristics of the action potential", though the content there seems fine. Absolutely no external links is not ideal, though there may be nothing worth linking to on such an esoteric topic. I'm also unsure about the "Related topics" section. All in all, though, the article has improved, and this review should pass, preferably with these issues addressed.
Tuf-Kat
09:56, 17 November 2005 (UTC)
-- maclean25 22:15, 22 November 2005 (UTC)
When reading the article from a signal processing POV, there are probably citations for the characteristic impedance of the axons, from Node to Node. The sentences hit all around the concept that there is a similarity between a transmission line and an axon, such as the statement that an action potential's shape is preserved as the pulse propagates down the axon. That is transmission line behavior. -- Ancheta Wis 00:45, 6 December 2005 (UTC)
I think this article would benefit from a bit more information on the mathematics of action potential velocity due to membrane capacitance and axonal resistance, and how these are affected by the diameter and myelination of the axon. While the "Detailed mechanism" section talk about capacitance, it doesn't mention resistance, which also has a an important role. Comparing the invertebrate and vertebrate methods of increasing action potential velocity is a good way of explaining this topic as it shows the interaction between membrane thickness and axonal diameter (and hence membrane capacitance and axonal resistance). I can add this information, including equations and examples of action potential velocities at different diameters, but thought I check to see what everyone else thinks first... I'm new to this! Hbdgaz 16:52, 11 December 2005 (UTC)
Simplyloic ( talk · contribs) has made some substantial edits to the "Underlying mechanism" section. They're much appreciated, but might be a sliver short of featured quality. A few more eyes doing some fact checking and copyediting would be much appreciated. I'll see about merging the new material with what was there previously (see [1]) as well. Cheers, David Iberri ( talk) 12:05, 7 April 2006 (UTC)
The traditional current circulation is from the + pole to negative one. The real current circulation is from negative pole to positive. The T4 phase of the picture shows a green arrow (circulation) that doesn't respect the rules used in the previous phases.-- Somasimple 04:57, 8 October 2007 (UTC)
Here is the error!
in the Detailed mechanism
Hi all, I think that the explanation fails with known facts? If speed seems to be linked with capacitance and if low capacitance promotes speed, why are large fibres (whith large capacitance) quicker than small ones? There is a contradiction? -- Somasimple 05:26, 21 June 2006 (UTC)
Hi David,
Hmm, If capacitance is the abillity to store charge then large unmyelinated fibres may get perhaps a lower internal resistance but a larger capacitance. It is a physical rule => diameter increased = more circumference and more charges allowed to stick on the membrane. It is a known fact that the growth curve of speed/diameter is quite a power of 0.6. It shows a slope decrease for large unmyelinated fibres. It is just why nature invented myelinated fibres. So I think that larges fibres (unmyelinated) have larger capacitance than smaller ones. In that case, the statement saying that capacitance is the key issue becomes wrong for unmyelinated fibres because small fibers comparatively are faster.-- Somasimple 17:05, 21 June 2006 (UTC)
Given two equally myelinated/unmyelinated axons...the key factor determining AP propagation speed is axon diameter (ie, internal resistance)
Not sure, because you changed a key factor: the physical resistance of the axon enveloppe. It is well known that unmyelinated fibres bulge during AP propagation. Increasing the thickness of membrane is a way to workaround this "problem".
Secondly, It is well known that exhanges during APs are done in a thin superficial layer => The internal resistance becomes less important.
Thirdly, in unmyelinated, we could say that "communication" occurs perpendicularly to the axon membrane. In meylinated, horizontal communication is favored. Could we conclude that Nature used the same means in the two solutions?
AP propagation occurs through the movement of charges. I agree totally in unmyelinated fibres since ions are charged particles moving physically. But since we know that they can't travel so far, how do you understand the movement charge within myelinated fibers?-- Somasimple 04:59, 22 June 2006 (UTC)
In the figure of propagation, you shows a T4 time with a backward current made impossible by the real nature of AP. Since Ap is a travelling wave then all points exist at the time and thus your left points are ever more positive when you consider the start of the curve. If we get more positive charges on the left, positive ions can't go there.-- Somasimple 14:18, 21 June 2006 (UTC) here is flash anim showing the ingoing positive charges making impossible the left current. [2] -- Somasimple 14:22, 21 June 2006 (UTC)
Transmission through an axon is not the same as transmission through a copper cable, true, but it is equivalent of transmission through an ionic solution where the solution is partly insulated via a semi permeable membrane. The effects of the specific membrane resistance and capacitance are to basically cause some of this current to leak out, limiting how far the current can spread down the axon. Both time constants and length constants have been measured empirically and can be predicted by properties such as membrane resistance and membrane capacitance, thus a cable analogy is useful. Measurements of conduction velocities in a wide range of nerve cells have been shown to correlate closely to their calculated resistances and capacitances. Nrets 15:45, 23 June 2006 (UTC)
Nrets, you do not listen to me. An AP is a travelling wave. If its speed is v1 at node and v2 under myelin (with v2>v1) AND because it is travelling wave AND thus a continuous phenomenon, every point of the curve MUST be dilated while changing medium. IT IS NOT WHAT SCIENTISTS RECORDED. THE SHAPE OF THE AP IS PRESERVED. CONCLUSION => the shape is not really transmitted. The wave is not travelling under the myelin. I have already read the Benazilla's stuff. A great scientist but too electrical.-- Somasimple 04:40, 28 June 2006 (UTC)
You wrote:"I'd be very interested to see some references to studies which show direct evidence that AP conduction velocity cannot be predicted by passive and active membrane properties.". Nrets, since AP occurs in an axon nobody can ;-) You can follow my foolish discussion on my site. You're welcome! ps: I have clues and proves.-- Somasimple 04:01, 29 June 2006 (UTC)
"Action potentials are an essential carrier of the neural code." I think Wikipedia:Explain jargon is in order. -- JWSchmidt 02:53, 22 June 2006 (UTC)
The introduction has one whole paragraph on the electrical signals in plants but nothing in the main text. While this is intereting and relevant this text should be moved from the introduction to the main text. The introduction is supposed to be a summary, not a place for new information. Alternatively a much larger section on electrical signals in plants should be incorporated into the article. Personally i think it would be enough to remove the text from the introduction. This topic should be mentioned in the main text but refer to a separate article. David D. (Talk) 15:51, 23 June 2006 (UTC)
Should these two be mentioned in the article as they make an action potential more/less likely (respectively)? dr.alf 09:09, 1 October 2006 (UTC)
Do you suppose it's worth saying anything about the fact that Hodgkin & Huxley got the Nobel prize for figuring out how action potentials work?
It seems odd that the idealized sketch of an action potential has a rising phase that is so slow compared with its falling phase. It also seems odd for this figure to have such a salient line labeled "threshold"--as if there is such a thing as "the" threshold for triggering a spike.
This statement "the threshold of an action potential is not the voltage at which sodium current becomes significant; it is the point where it exceeds the potassium current." is true only for a membrane action potential (i.e. only for a nonpropagating spike in an isolated patch of membrane). It is not true for action potentials that arise at a "trigger zone" in a physically extended structure, such as a neuron (or even an axon).
"An action potential is a rapid swing in the polarity of the voltage from negative to positive and back, the entire cycle lasting a few milliseconds. Each cycle—and therefore each action potential—has a rising phase, a falling phase, and finally an undershoot" Except for those cells that have broad action potentials, e.g. cardiac muscle.
The following statement is meaningless: "The natural tendency of sodium and potassium ions is to diffuse across their electrochemical gradients to attempt to reach their respective equilibrium potentials"
If "the resting cell membrane is approximately 100 times more permeable to potassium than to sodium, so that more potassium diffuses out of the cell than sodium diffuses in", then how can a pump with 3:2 stoichiometry maintain the cell in steady state?
"the dominant outward leak of potassium ions produces a hyperpolarizing current that establishes the cell's resting potential of roughly -70 mV." A cell at rest has a net hyperpolarizing transmembrane current?
If "inward and outward currents are equal," net transmembrane current is 0, not hyperpolarizing.
"Establishment of a membrane potential of around +40 mV closes the voltage-sensitive inactivation gates of the sodium channels, which are sensitive to the now-positive membrane potential gradient, preventing further influx of sodium. While this occurs, the voltage-sensitive activation gates on the voltage-gated potassium channels begin to open." Which implies the following totally incorrect conclusions:
1. sodium current turns off at, or shortly after, the peak of the spike
The statement "Establishment of a membrane potential of around +40 mV closes the voltage-sensitive inactivation gates of the sodium channels . . . preventing further influx of sodium" is false.
A. "According to the H&H model it does." Not so. Sodium current does not turn off at the peak of the spike, or shortly after the peak. In fact, not only does it continue to increase for quite some time after the peak of the spike, (1) the maximum sodium current (which occurs during the falling phase of the spike) is almost twice as big as the value at the peak of the spike, and (2) about 80% of the sodium influx during a spike occurs _after_ the peak. B. "After the Na+ channels inactivate, the Na+ conductance starts to decrease." Again not so. Inactivated channels are closed channels. Closed channels have zero conductance. Their conductance does not "start to decrease after they inactivate." And in the HH model, sodium conductance continues to increase for a bit after the peak of the spike.
2. most of the sodium influx during a spike occurs before the depolarized peak; very little enters after the peak
The statement is that "Establishment of a membrane potential of around +40 mV closes the voltage-sensitive inactivation gates of the sodium channels . . . preventing further influx of sodium"? This is a clear assertion that the sodium channels close and no more sodium influx can occur. It does not say that some channels remain open.
3. sodium current dwarfs potassium current during the rising phase of the spike
The delay is only slight. At the point of maximum slope on the rising phase of the spike, potassium current is already about 20% as large as sodium current. And it catches up quickly--at the peak of the spike, the currents are nearly equal.
[Action potentials] "are often modeled using hypothetical cells containing only two transmembrane ion channels (a voltage-gated sodium channel and a non-voltage-gated potassium channel)."
Citation please. Somewhere or other in this article, one might expect to see the
Hodgkin-Huxley model mentioned, too, if merely as a counterexample.
The discussion of IV curves lacks clarity.
"The main impediment to conduction speed in unmyelinated axons is membrane capacitance." Whatever happened to cytoplasmic resistivity? By the way, cytoplasmic resistivity accounts for the effect of axon diameter on conduction velocity.
Membrane capacitance would have no effect on conduction velocity if it were not for cytoplasmic resistivity. That's a consequence of the laws of physics, not a matter about which feelings have any relevance.
[Myelination] "allows the rapid (essentially instantaneous) conduction of ions through a myelinated segment of axon" Not so. Ionic mobility is very slow--far slower than the action potential.
Bear et al., Kandel's books, and Purvis et al. are very weak on this stuff. Aidley (The Physiology of Excitable Cells) is a far superior text, to name just one.
I could be wrong, but isn't this passage incorrect?
An action potential is a rapid swing in the polarity of the voltage from positive to negative and back, the entire cycle lasting a few milliseconds.
Maybe I'm just confused about action potentials, but I thought that the resting potential voltage was negative, then when the action potential came along, there is depolarisation to a positive value, then repolarisation back to negative. So surely it should be:
An action potential is a rapid swing in the polarity of the voltage from negative to positive and back, the entire cycle lasting a few milliseconds.
-- Jen1502 12:45, 28 January 2007 (UTC)
It all depends on your point of reference. In modern nomenclature, the resting potential of a typical neuron (inside relative to outside) is negative (~60-70mV). However, in the original J. Physiology papers by H-H, they use the opposite reference point (outside relative to inside) hence the resting potential starts positive and the AP causes a transient drop in the potential. This is probably where the confusion comes in (It gets new 1st time readers of those papers every time...)
AndrewHires 18:09, 12 February 2007 (UTC)
Leaving record of old FARC which was never correctly archived here. SandyGeorgia ( Talk) 17:47, 3 February 2007 (UTC)
That's correct, HH reversed the current flow convention, but not the polarity. The inside is, in fact, negative relative to the outside. —Preceding unsigned comment added by Synaptidude ( talk • contribs) 19:44, 1 November 2007 (UTC)
[3] This article seems to suggest that it is sound waves, not electrical impulses which are propagating. Can anyone confirm? If so, much of this article would seem to now be incorrect. Cariaso 22:54, 6 March 2007 (UTC)
can someone provide a reference for plant actin potential. i've never come across this, i sounds facinating! oh yeah and because that section is unreferenced as well i guess.-- Dylan2106 10:50, 14 May 2007 (UTC)
It seems to me that part B of the image RC_membrane_circuit.jpg is wrong. It should be like for example here: http://biology.unm.edu/toolson/b435/equivcirc.html, the batteries in series with the resistors (channels).
The traditional current circulation is from the + pole to negative one. The real current circulation is from negative pole to positive. The T4 phase of the picture shows a green arrow (circulation) that doesn't respect the rules used in the previous phases.-- Somasimple 06:50, 9 October 2007 (UTC)
I corrected some nomenclature in the article. Voltage-gated sodium channels (and others as well) exist in at least three states: Open, Closed, and Inactivated. In a classic Markov model, there are even more states needed to account for the kinetics that arise from the fact that each channel has more than one activation gate and more than one inactivation gate. Two activation gates (A1 and A2), for example, where both need to be "open" to have the channel itself be open, means that there are three closed states: A1 AND A2 closed, A1 open A2 closed, and A1 closed A2 open). However, for the sake of simplicity, one can assert that "closed" is a single state of the holochannel. So for these three states (that may encompass numbers of sub-states): Open is open. Deactivated is closed but available to open, Inactivated is closed and unable to open. In the article the Inactivated state was called "deactivated". This is not the usual convention.
I also deleted on parenthetical statement that made no sense, but I've forgotten what it was, so I'll have to go back to the history to document it. Synaptidude —Preceding comment was added at 19:53, 1 November 2007 (UTC)
This statement:
The Hodgkin-Huxley model for action potential firing described above derives its principle evidence from Voltage-Clamping experiments on giant squid axons.
was kind of hanging out as a non-sequiter in the 'refractory period' section. There should probably be a section devoted to the contribution of H & H. Synaptidude 01:22, 8 November 2007 (UTC)
![]() | This page is an archive of past discussions. Do not edit the contents of this page. If you wish to start a new discussion or revive an old one, please do so on the current talk page. |
"An action potential is an electrical pulse that changes the voltage (potential) across a cell membrane. In muscle and nerve cells, this rapid change in voltage leads to an action such as muscular contraction or neurotransmitter release. These actions are usually a consequence of calcium ions entering the cell during the rapid change in voltage. "
I think any definition has to include the idea of propagation, if not the idea of a wave, which is the mode of propagation in the first kind of action potential most people think of, which is in nerves. It's just wrong that calcium "usually" causes an AP. According to the Hodgkin-Huxley theory, based on the way things work in the giant axon of the squid, all you need are sodium channels and potassium channels. Calcium is important in coupling excitation (the AP) to contraction in muscle, but at the neuromuscular junction its acetylcholine receptors that initiate the action potential, and these will predominantly be carrying sodium into the cell. I suspect they don't permit calcium at all.
Maybe I'm being pedantic here, but if you look at the phrase "action potential", it is clearly a noun. It should refer to the level of potential necessary to incite action (or some similar aspect of the amount of potential), not the process of changing potential. Is all of neurochemistry suffering a semantic deficit, or just this article? p.s. I'm coming from an electronics background, where potential clearly means "voltage" -- which, in this case, it literally does, so I think I'm standing on solid semantic ground. 12.210.113.235 14:20, 1 June 2006 (UTC)
What does the cartoon of the phospholipid membrane have to do with an action potential? There aren't even any ion channels in the drawing, as far as I could tell. Could someone find a nice graph of an action potential (i.e. a voltage-time graph showing membrane potential increasing to threshold, then firing, then a refractory period)? Sayeth 19:52, Jul 29, 2004 (UTC)
I agree the top picture should be a voltage-time graph. Perhaps when one is found the membrane image could move further down the article? Richard Taylor
Thanks for the new caption, Richard. It makes the drawing much more relevant, but I agree that there's still some improvement possible with a second picture. Sayeth 19:52, Jul 29, 2004 (UTC)
I had a few minutes of spare time and decided to redraw Chris' image in Adobe Illustrator. It's basically the same image with some antialiasing and smaller font sizes for readability. Would anyone object if I replaced the current image with my version? -- Diberri | Talk 17:22, Jul 30, 2004 (UTC)
Is the refractory period a) that long and b) is the hyperpolarisation so "hyper" (ie does it go so negative?). I thougth that both were smaller. Batmanand 14:16, 22 Jun 2005 (UTC)
Hi this article no longer meets the criteria for a featured article because it does not cite its sources. Please help fix this so that all featured articles can meet the same standards. Best would be the most trusted resources in the field being added, some print resources especially, but also online references are better than none. Those sources would likely help with good material to further improve the article anyway. - Taxman 23:00, Oct 26, 2004 (UTC)
I'm familiar with the contents of Kandel, X and Schwartz. Yes, the content of that one aggrees with what is said here. I've not read Bear (although he did once hit on my girlfriend ;-), but this is all such "textbook stuff" that I'm sure Bear also supports what is in here.
I've also added references to the primary literature: the original HH papers and also an updated look at HH-models. Synaptidude 5 July 2005 20:58 (UTC)
The first paragraph reads:
What is the evidence that the speed of an action potential contrains the size of an organism or organ? It is not discussed in the article.
Also, there are propagating action potentials in plants. They can move along the phloem cell membranes similar to nerves. A good example of this is the sensitive mimosa plant. It's leaflets close in response to touch and the movement can be seen to propagate down the stem. This is due to motor cells sequentially releasing water due to the change in membrane potential as the action potential progress' down the stem. This was observed and published by Charles Darwin in his less famous book The power of movement in plants. John Murray, London, 1880. There are two big differences between plant and animal action potentials: 1) plant AP's are much slower; 2) plant AP's are generated with K+ and anions, unlike animals that use K+ and Na+ ions. David D. 15:32, 3 May 2005 (UTC)
You know, you could argue for days on end about chicken/egg aspects of evolutionary changes. I'm completely unfamiliar with any literature on action potentials and evolution, and yet it would seem obvious that the relationship between the two will be complex, probably showing causality in both directions (i.e. action potential propagation limits body size at the same time that body size limits axon diameter. Since evolutionary statements such as the one made in this article are often just informed speculation anyway, this whole problem can be (and has been) fixed by using the all-purpose scientist solution: "when you've got a feasible idea that you can't prove, say "may". Synaptidude 5 July 2005 21:05 (UTC)
I relabeled the graph showing the voltage-time relationships of the action potential. The former labels were slightly misleading in the following ways. 1) "Depolarization" and "Hyperpolarization" have been replaced with "Rising" and "Falling Phase". First, these are the correct terminologies in use by electrophysiologists. Second, the Rising Phase, once it crosses 0 mV is actually hyperpolarizing (see hyperpolarization. Likewise, the falling phase before it reaches 0 mV is actually depolarizing (see depolarization). This is why electrophysiologists don't use those terms to describe the rising and falling phases (each is a mixed hyper/depolarization). 2) The label "Refractory Period" has been replaced by "Undershoot". This is because the label incorrectly implied that the undershoot of membrane potental at the end of the action potential is the basis for the refractory period. The basis for the refractory period is actually a change in the action potential threshold caused by sodium channel inactivation (which has nothing directly to do with the undershoot). The undershoot is actually too large in this diagram, but I decided not to fix this at this time. According to the voltage scale used, the undershoot would go to approx. -100 mV. This is below Ek, and therefore physically impossible. 3)I've added ~ marks to the voltage scale of the y-axis. This is to indicate that the values of resting, threshold and peak potentials are approximate. For example, neurons rest anywhere from -80 to -55 mV. Thresholds and peaks vary similarly. 4) I've added a label for "overshoot", that is, the part of the action potential that overshoots 0 mV. Synaptidude 5 July 2005 18:59 (UTC)
Yes, thanks. I see that now. I guess it's time to do something about it. Synaptidude 5 July 2005 21:10 (UTC)
I'll have to check, but I think it was more likely Cole than H&H who "discovered" the propagating nature of action potentials. I think one could actually make a pretty strong argument for Sherington, who certainly knew that nerve impulses were propagated, although he didn't know specifically about action potentials per se
I suggest putting Part A and Part B of the first figure like this:
A
B
As it is now, it is leaving too little room for the main text along the left side of the page. -- Memenen 9 July 2005 16:52 (UTC)
simplicity ? -- AHands 21:39, 10 August 2005 (UTC)
Your childish vandalism of this article has been noted and reported to your ISP, as well as your parents. Synaptidude 23:48, 21 November 2005 (UTC)
Reading the suggestions in the featured review section, I have undertaken some changes (hope they are improvments)
1) I've re-written the introduction to make it more general and accurate. The accuracy part is the the "sets the pace of thought" statement. I have removed this because there is no evidence for this. Most current thought is that the pace of thought is set by the speed of neural osicillators that are made of networks of many neurons. While action potentials certainly subserve parts of the function of these oscillators, they are not the rate-limiting steps. It would be no more accurate to say that the frequencies coming from a radio speaker are set by the speed of electron travel through copper. Synaptidude 00:11, 22 November 2005 (UTC)
2) made some changes to clarify and more accurately reflect how the action potential is initiated
3) Added a section of "Why" the body uses action potentials
more to come Synaptidude 01:45, 22 November 2005 (UTC)
I flipped over to this Talk page to make some witty comment about how in depth this article is, and then I noticed it's a featured article...someone really knows their stuff heh
This was the version promoted in February of 2004, and
these are the changes made since. Article has been completely rewritten. The new version is quite a bit longer, and appears to be more comprehensive. The only significant issue I see is the diagram next to the lead, which makes for some very bad formatting (the lead is squeezed into really, really short lines), and the diagram seems a bit complex for the lead anyway (though I recognize this was likely done because no real image could be used for this article). Also, I don't like the section heading "Noteworthy characteristics of the action potential", though the content there seems fine. Absolutely no external links is not ideal, though there may be nothing worth linking to on such an esoteric topic. I'm also unsure about the "Related topics" section. All in all, though, the article has improved, and this review should pass, preferably with these issues addressed.
Tuf-Kat
09:56, 17 November 2005 (UTC)
-- maclean25 22:15, 22 November 2005 (UTC)
When reading the article from a signal processing POV, there are probably citations for the characteristic impedance of the axons, from Node to Node. The sentences hit all around the concept that there is a similarity between a transmission line and an axon, such as the statement that an action potential's shape is preserved as the pulse propagates down the axon. That is transmission line behavior. -- Ancheta Wis 00:45, 6 December 2005 (UTC)
I think this article would benefit from a bit more information on the mathematics of action potential velocity due to membrane capacitance and axonal resistance, and how these are affected by the diameter and myelination of the axon. While the "Detailed mechanism" section talk about capacitance, it doesn't mention resistance, which also has a an important role. Comparing the invertebrate and vertebrate methods of increasing action potential velocity is a good way of explaining this topic as it shows the interaction between membrane thickness and axonal diameter (and hence membrane capacitance and axonal resistance). I can add this information, including equations and examples of action potential velocities at different diameters, but thought I check to see what everyone else thinks first... I'm new to this! Hbdgaz 16:52, 11 December 2005 (UTC)
Simplyloic ( talk · contribs) has made some substantial edits to the "Underlying mechanism" section. They're much appreciated, but might be a sliver short of featured quality. A few more eyes doing some fact checking and copyediting would be much appreciated. I'll see about merging the new material with what was there previously (see [1]) as well. Cheers, David Iberri ( talk) 12:05, 7 April 2006 (UTC)
The traditional current circulation is from the + pole to negative one. The real current circulation is from negative pole to positive. The T4 phase of the picture shows a green arrow (circulation) that doesn't respect the rules used in the previous phases.-- Somasimple 04:57, 8 October 2007 (UTC)
Here is the error!
in the Detailed mechanism
Hi all, I think that the explanation fails with known facts? If speed seems to be linked with capacitance and if low capacitance promotes speed, why are large fibres (whith large capacitance) quicker than small ones? There is a contradiction? -- Somasimple 05:26, 21 June 2006 (UTC)
Hi David,
Hmm, If capacitance is the abillity to store charge then large unmyelinated fibres may get perhaps a lower internal resistance but a larger capacitance. It is a physical rule => diameter increased = more circumference and more charges allowed to stick on the membrane. It is a known fact that the growth curve of speed/diameter is quite a power of 0.6. It shows a slope decrease for large unmyelinated fibres. It is just why nature invented myelinated fibres. So I think that larges fibres (unmyelinated) have larger capacitance than smaller ones. In that case, the statement saying that capacitance is the key issue becomes wrong for unmyelinated fibres because small fibers comparatively are faster.-- Somasimple 17:05, 21 June 2006 (UTC)
Given two equally myelinated/unmyelinated axons...the key factor determining AP propagation speed is axon diameter (ie, internal resistance)
Not sure, because you changed a key factor: the physical resistance of the axon enveloppe. It is well known that unmyelinated fibres bulge during AP propagation. Increasing the thickness of membrane is a way to workaround this "problem".
Secondly, It is well known that exhanges during APs are done in a thin superficial layer => The internal resistance becomes less important.
Thirdly, in unmyelinated, we could say that "communication" occurs perpendicularly to the axon membrane. In meylinated, horizontal communication is favored. Could we conclude that Nature used the same means in the two solutions?
AP propagation occurs through the movement of charges. I agree totally in unmyelinated fibres since ions are charged particles moving physically. But since we know that they can't travel so far, how do you understand the movement charge within myelinated fibers?-- Somasimple 04:59, 22 June 2006 (UTC)
In the figure of propagation, you shows a T4 time with a backward current made impossible by the real nature of AP. Since Ap is a travelling wave then all points exist at the time and thus your left points are ever more positive when you consider the start of the curve. If we get more positive charges on the left, positive ions can't go there.-- Somasimple 14:18, 21 June 2006 (UTC) here is flash anim showing the ingoing positive charges making impossible the left current. [2] -- Somasimple 14:22, 21 June 2006 (UTC)
Transmission through an axon is not the same as transmission through a copper cable, true, but it is equivalent of transmission through an ionic solution where the solution is partly insulated via a semi permeable membrane. The effects of the specific membrane resistance and capacitance are to basically cause some of this current to leak out, limiting how far the current can spread down the axon. Both time constants and length constants have been measured empirically and can be predicted by properties such as membrane resistance and membrane capacitance, thus a cable analogy is useful. Measurements of conduction velocities in a wide range of nerve cells have been shown to correlate closely to their calculated resistances and capacitances. Nrets 15:45, 23 June 2006 (UTC)
Nrets, you do not listen to me. An AP is a travelling wave. If its speed is v1 at node and v2 under myelin (with v2>v1) AND because it is travelling wave AND thus a continuous phenomenon, every point of the curve MUST be dilated while changing medium. IT IS NOT WHAT SCIENTISTS RECORDED. THE SHAPE OF THE AP IS PRESERVED. CONCLUSION => the shape is not really transmitted. The wave is not travelling under the myelin. I have already read the Benazilla's stuff. A great scientist but too electrical.-- Somasimple 04:40, 28 June 2006 (UTC)
You wrote:"I'd be very interested to see some references to studies which show direct evidence that AP conduction velocity cannot be predicted by passive and active membrane properties.". Nrets, since AP occurs in an axon nobody can ;-) You can follow my foolish discussion on my site. You're welcome! ps: I have clues and proves.-- Somasimple 04:01, 29 June 2006 (UTC)
"Action potentials are an essential carrier of the neural code." I think Wikipedia:Explain jargon is in order. -- JWSchmidt 02:53, 22 June 2006 (UTC)
The introduction has one whole paragraph on the electrical signals in plants but nothing in the main text. While this is intereting and relevant this text should be moved from the introduction to the main text. The introduction is supposed to be a summary, not a place for new information. Alternatively a much larger section on electrical signals in plants should be incorporated into the article. Personally i think it would be enough to remove the text from the introduction. This topic should be mentioned in the main text but refer to a separate article. David D. (Talk) 15:51, 23 June 2006 (UTC)
Should these two be mentioned in the article as they make an action potential more/less likely (respectively)? dr.alf 09:09, 1 October 2006 (UTC)
Do you suppose it's worth saying anything about the fact that Hodgkin & Huxley got the Nobel prize for figuring out how action potentials work?
It seems odd that the idealized sketch of an action potential has a rising phase that is so slow compared with its falling phase. It also seems odd for this figure to have such a salient line labeled "threshold"--as if there is such a thing as "the" threshold for triggering a spike.
This statement "the threshold of an action potential is not the voltage at which sodium current becomes significant; it is the point where it exceeds the potassium current." is true only for a membrane action potential (i.e. only for a nonpropagating spike in an isolated patch of membrane). It is not true for action potentials that arise at a "trigger zone" in a physically extended structure, such as a neuron (or even an axon).
"An action potential is a rapid swing in the polarity of the voltage from negative to positive and back, the entire cycle lasting a few milliseconds. Each cycle—and therefore each action potential—has a rising phase, a falling phase, and finally an undershoot" Except for those cells that have broad action potentials, e.g. cardiac muscle.
The following statement is meaningless: "The natural tendency of sodium and potassium ions is to diffuse across their electrochemical gradients to attempt to reach their respective equilibrium potentials"
If "the resting cell membrane is approximately 100 times more permeable to potassium than to sodium, so that more potassium diffuses out of the cell than sodium diffuses in", then how can a pump with 3:2 stoichiometry maintain the cell in steady state?
"the dominant outward leak of potassium ions produces a hyperpolarizing current that establishes the cell's resting potential of roughly -70 mV." A cell at rest has a net hyperpolarizing transmembrane current?
If "inward and outward currents are equal," net transmembrane current is 0, not hyperpolarizing.
"Establishment of a membrane potential of around +40 mV closes the voltage-sensitive inactivation gates of the sodium channels, which are sensitive to the now-positive membrane potential gradient, preventing further influx of sodium. While this occurs, the voltage-sensitive activation gates on the voltage-gated potassium channels begin to open." Which implies the following totally incorrect conclusions:
1. sodium current turns off at, or shortly after, the peak of the spike
The statement "Establishment of a membrane potential of around +40 mV closes the voltage-sensitive inactivation gates of the sodium channels . . . preventing further influx of sodium" is false.
A. "According to the H&H model it does." Not so. Sodium current does not turn off at the peak of the spike, or shortly after the peak. In fact, not only does it continue to increase for quite some time after the peak of the spike, (1) the maximum sodium current (which occurs during the falling phase of the spike) is almost twice as big as the value at the peak of the spike, and (2) about 80% of the sodium influx during a spike occurs _after_ the peak. B. "After the Na+ channels inactivate, the Na+ conductance starts to decrease." Again not so. Inactivated channels are closed channels. Closed channels have zero conductance. Their conductance does not "start to decrease after they inactivate." And in the HH model, sodium conductance continues to increase for a bit after the peak of the spike.
2. most of the sodium influx during a spike occurs before the depolarized peak; very little enters after the peak
The statement is that "Establishment of a membrane potential of around +40 mV closes the voltage-sensitive inactivation gates of the sodium channels . . . preventing further influx of sodium"? This is a clear assertion that the sodium channels close and no more sodium influx can occur. It does not say that some channels remain open.
3. sodium current dwarfs potassium current during the rising phase of the spike
The delay is only slight. At the point of maximum slope on the rising phase of the spike, potassium current is already about 20% as large as sodium current. And it catches up quickly--at the peak of the spike, the currents are nearly equal.
[Action potentials] "are often modeled using hypothetical cells containing only two transmembrane ion channels (a voltage-gated sodium channel and a non-voltage-gated potassium channel)."
Citation please. Somewhere or other in this article, one might expect to see the
Hodgkin-Huxley model mentioned, too, if merely as a counterexample.
The discussion of IV curves lacks clarity.
"The main impediment to conduction speed in unmyelinated axons is membrane capacitance." Whatever happened to cytoplasmic resistivity? By the way, cytoplasmic resistivity accounts for the effect of axon diameter on conduction velocity.
Membrane capacitance would have no effect on conduction velocity if it were not for cytoplasmic resistivity. That's a consequence of the laws of physics, not a matter about which feelings have any relevance.
[Myelination] "allows the rapid (essentially instantaneous) conduction of ions through a myelinated segment of axon" Not so. Ionic mobility is very slow--far slower than the action potential.
Bear et al., Kandel's books, and Purvis et al. are very weak on this stuff. Aidley (The Physiology of Excitable Cells) is a far superior text, to name just one.
I could be wrong, but isn't this passage incorrect?
An action potential is a rapid swing in the polarity of the voltage from positive to negative and back, the entire cycle lasting a few milliseconds.
Maybe I'm just confused about action potentials, but I thought that the resting potential voltage was negative, then when the action potential came along, there is depolarisation to a positive value, then repolarisation back to negative. So surely it should be:
An action potential is a rapid swing in the polarity of the voltage from negative to positive and back, the entire cycle lasting a few milliseconds.
-- Jen1502 12:45, 28 January 2007 (UTC)
It all depends on your point of reference. In modern nomenclature, the resting potential of a typical neuron (inside relative to outside) is negative (~60-70mV). However, in the original J. Physiology papers by H-H, they use the opposite reference point (outside relative to inside) hence the resting potential starts positive and the AP causes a transient drop in the potential. This is probably where the confusion comes in (It gets new 1st time readers of those papers every time...)
AndrewHires 18:09, 12 February 2007 (UTC)
Leaving record of old FARC which was never correctly archived here. SandyGeorgia ( Talk) 17:47, 3 February 2007 (UTC)
That's correct, HH reversed the current flow convention, but not the polarity. The inside is, in fact, negative relative to the outside. —Preceding unsigned comment added by Synaptidude ( talk • contribs) 19:44, 1 November 2007 (UTC)
[3] This article seems to suggest that it is sound waves, not electrical impulses which are propagating. Can anyone confirm? If so, much of this article would seem to now be incorrect. Cariaso 22:54, 6 March 2007 (UTC)
can someone provide a reference for plant actin potential. i've never come across this, i sounds facinating! oh yeah and because that section is unreferenced as well i guess.-- Dylan2106 10:50, 14 May 2007 (UTC)
It seems to me that part B of the image RC_membrane_circuit.jpg is wrong. It should be like for example here: http://biology.unm.edu/toolson/b435/equivcirc.html, the batteries in series with the resistors (channels).
The traditional current circulation is from the + pole to negative one. The real current circulation is from negative pole to positive. The T4 phase of the picture shows a green arrow (circulation) that doesn't respect the rules used in the previous phases.-- Somasimple 06:50, 9 October 2007 (UTC)
I corrected some nomenclature in the article. Voltage-gated sodium channels (and others as well) exist in at least three states: Open, Closed, and Inactivated. In a classic Markov model, there are even more states needed to account for the kinetics that arise from the fact that each channel has more than one activation gate and more than one inactivation gate. Two activation gates (A1 and A2), for example, where both need to be "open" to have the channel itself be open, means that there are three closed states: A1 AND A2 closed, A1 open A2 closed, and A1 closed A2 open). However, for the sake of simplicity, one can assert that "closed" is a single state of the holochannel. So for these three states (that may encompass numbers of sub-states): Open is open. Deactivated is closed but available to open, Inactivated is closed and unable to open. In the article the Inactivated state was called "deactivated". This is not the usual convention.
I also deleted on parenthetical statement that made no sense, but I've forgotten what it was, so I'll have to go back to the history to document it. Synaptidude —Preceding comment was added at 19:53, 1 November 2007 (UTC)
This statement:
The Hodgkin-Huxley model for action potential firing described above derives its principle evidence from Voltage-Clamping experiments on giant squid axons.
was kind of hanging out as a non-sequiter in the 'refractory period' section. There should probably be a section devoted to the contribution of H & H. Synaptidude 01:22, 8 November 2007 (UTC)