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The article is extremely confusing, there is a lot of material and definitions which are, however, poorly organized. A lot of repetitions and the flow of argument is completely absent. I'll see what i can do.
It is incredible that it is a FEATURED ARTICLE with so many problems
Rvfrolov (
talk)
18:32, 2 January 2009 (UTC) 2 January 2009
There are three articles now which discuss very much the same things with numerous repetitions and description of the same material in different terms.
As it was already suggested by Methoxyroxy 12:37, 2 November 2006 (UTC), it needs a really big clean-up and optimization. There is a lot of confusion there so I will do this albeit not at once. I will move different parts between these three articles, edit and unify their style etc. At later stage I will need someone who is native English speaker to do spellcheck. Rvfrolov ( talk) 20:52, 2 January 2009 (UTC)
The current version of the article mixes action potentials with propagation of potentials creating excessive complexity and inaccuracies.
Potential propagation is not a required property of an action potential. Most textbooks first define the action potential in an isopotential cell. In Hodkin and Huxley's experiments, for example, a wire was strung along a squid giant axon to shunt axial currents effectively producing an isopotential membrane compartment. With this preparation, current-clamp experiments still produce action potentials along the entire fiber, without a "wave of electrochemical activity." Neither does a cell need to carry APs over a distance to make use of action potentials (e.g. electrocyte action potentials in electric fish, and many other cell types produce action potentials for other reasons than long-distance signaling).
The current definition is also missing a key defining component: the key role of voltage-sensitive conductances.
Propagating action potentials may be more consistently described as a continuous succession of local action potentials triggering action potentials in the adjacent sections. This distinction would help avoid some of the current inaccuracies in the article.
For example, the current article describes saltatory conduction as follows "Since the axon is insulated, the action potential can travel through it without significant signal decay." In reality, myelinated stretches of axons do not produce action potentials and the action potential does not "travel through it." It would be more accurate to state that depolarization from an action potential at one node propagates passively to the next node and triggers an action potential at the next node. The signal may decay significantly between nodes and still trigger an action potential at the next node. The same section seems to imply that the action potential must be generated at the synapse for the release of neurotransmitter, which is also inaccurate. Any depolarization of sufficient magnitude (passive or active) will have a similar effect.
In summary, to make the article more useful, I recommend providing a complete and general definition of the action potential with minimal extraneous detail. The adjacent topics such as "Electrotonic propagation of potentials", "Neurotransmitter release", "Cable theory", "Saltatory conduction", probably belong in separate articles or sections.
Yatsenko DV ( talk) 03:45, 27 July 2009 (UTC)
I am removing "nerve spikes" from the first sentence.
I do not believe that the term "nerve spike" could be generally applied to all action potentials. Action potentials are transient membrane voltage events in individual cells or their compartments. They happen in many cell types. Nerves are bundles of axons in the peripheral nervous system (no nerves in the brain or spinal cord). Thus "nerve spikes" are but one specific manifestation of action potentials. The same could be said about MUAPs (motor unit action potentials), for example. This does not make them synonymous with action potentials. Dimitri Yatsenko 01:25, 28 July 2009 (UTC)
The current wording in the second paragraph states that depolarization "increases both the inward sodium current (depolarization) and the balancing outward potassium current (repolarization/hyperpolarization)". I question the accuracy of that statement.
As the membrane depolarizes, the membrane potential moves toward the reversal potential for sodium. This reduces the electrochemical driving force for sodium. Unless the sodium conductance increases by a greater factor to compensate, the sodium current will decrease, not increase. So the statement is not generally accurate. I propose rewording it to state that both conductances increase and only when the net current is negative and leads to further depolarization, a positive feedback loop is generated to precipitate the action potential. Dimitri Yatsenko 21:07, 28 July 2009 (UTC) —Preceding unsigned comment added by Yatsenko DV ( talk • contribs)
In the "Quantitative models" section there are many references to things being simple or a simplification. While this section does have many references attached to it, there is no mention in the article of what these things are simpler than. That is, why are these things simple, and compared to what, and what would be more complex.
The refractory period section seems like it was copy pasted from a text book which was written by a high school teach held at gun point. Perhaps we should consider updating it Paskari ( talk) 23:30, 6 October 2009 (UTC)
I've just attempted a pretty major rewrite of the lead, which I hope won't offend anybody. I thought the existing version was too hard for readers to understand -- it also contained a couple of minor errors. I also added a paragraph about the distinction between sodium and calcium spikes, which seems to me to be a very important point. Regards, Looie496 ( talk) 20:08, 23 February 2010 (UTC)
I have removed a reference from the lede that was to:
{{
cite book}}
: CS1 maint: multiple names: authors list (
link)Alphascript Publishing republished Wikipedia content. And the book in question republishes this article. The cover of the book can be seen [http://www.amazon.com/Cardiac-action-potential-Frederic-Miller/dp/6130098685/ref=sr_1_1?ie=UTF8&s=books&qid=1267362547&sr=1-1 on Amazon]. This article is named on the front cover. (The format for Alphascript books is to list the WP articles contained therein on the front cover as part of the name.)
The person who owns the book can verify that this is republished Wikipedia content by looking at the copyright information inside the book itself. -- RA ( talk) 13:16, 28 February 2010 (UTC)
The region with high concentration will diffuse out toward the region with low concentration. To extend the example, let solution A have 30 sodium ions and 30 chloride ions. Also, let solution B have only 20 sodium ions and 20 chloride ions. Assuming the barrier allows both types of ions to travel through it, then a steady state will be reached whereby both solutions have 25 sodium ions and 25 chloride ions. If, however, the porous barrier is selective to which ions are let through, then diffusion alone will not determine the resulting solution. Returning to the previous example, let's now construct a barrier that is permeable only to sodium ions. Since solution B has a lower concentration of both sodium and chloride, the barrier will attract both ions from solution A.
There is not a single citation about osmosis. Osmosis tells us exactly the contrary. Facts tells us the same thing as osmosis: The cited diffusion doesn't occur. The concentrations may be equilibrated by water movement and membrane is permeable to water through aquaporins or directly. Somasimple ( talk) 05:28, 3 June 2010 (UTC)
Secondly,
If solution A is electroneutral THEN 30n+30p=0 (where n stands for negative and p for positive). If solution B is also electroneutral THEN 25n+25p=0. Considering an action from a compartment onto another one orders to consider all positive and negative charges that exist in the compartments.
So, there is NO electric flux OR electric field BECAUSE EACH compartment is neutral at start. Saying a compartment is neutral is saying that it can't exert any electric "thing" at all.
Conclusion: You can't get something that is the result of k(25p/30p) or k(30p/25p). That is mathematically and physically incorrect because you arbitrarily remove the negative charges without any scientific explanation. Somasimple ( talk) 09:27, 3 June 2010 (UTC)
The inward movement of sodium ions and the outward movement of potassium ions are passive
Let's describe all the events that happen simultaneously:
1/ Sodium movement balanced with chloride
sodium is inward and Na ions stick to the internal membrane, chloride ions stay out, and balance the Na charge, across the external membrane
2/ Potassium movement balanced with chloride
potassium is outward and K ions stick to the external membrane, chloride ions stay in, and balance the K charge, across the internal membrane
Now let's see what happens on each side:
1/ Internal side:
sodium is inward and Na ions stick to the internal membrane, chloride ions stay in, and balance the K charge, across the internal membrane
2/ External side
chloride ions stay out, and balance the Na charge, across the external membrane, potassium is outward and K ions stick to the external membrane
Result: a membrane voltage that is... quite null.
Osmosis: Since there are concentrations changes there is water flux through aquaporins:
1/ from int to ext for sodium
2/ from ext to int for potassium
Result : How is it possible to make a bidirectional and simultaneous water movement in aquaporins? Somasimple ( talk) 05:57, 5 June 2010 (UTC)
About this section Myelin and saltatory conduction It is said:
The first assertion is false since every axon is covered by myelin; compact or not, leaving no room (<20 nm) around the axon. See the excellent book, page 128 [http://www.amazon.com/Neurocytology-Structure-Neurons-Processes-Neuroglial/dp/313781801X/ref=sr_1_1?ie=UTF8&s=books&qid=1276061846&sr=1-1 Neurocytology: Fine Structure of Neurons, Nerve Processes and Neuroglial Cells]
The second becomes, in that case, not true since it assumes that unmyelinated axons are bare. -- Somasimple ( talk) 05:43, 9 June 2010 (UTC)
In this article [
Cable Theory] the conduction velocity depends greatly of the time constant that is result of τm=Cm*Rm
It is said that myelin decreases the membrance capacitance. That's seems OK but what happens to the membrane resistance in case of myelinization?
Computation of the the time constant with reasonable values leads to an increase of the time constant:
You may see a
discussion about this problem.--
Somasimple (
talk)
10:55, 11 June 2010 (UTC)
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-- Tryptofish ( talk) 19:21, 11 June 2010 (UTC)
Everyone know this limitation. Does that mean that errors must NOT be discussed and thus articles, NOT improved?
I brought in the previous section a computation that contradicts the notion of velocity improvement by capacitance reduction of myelin. You get any rigth to bring another computation that tells something else or you MUST accept the fact that article formulation is wrong even if it contradicts your actual conviction. Here is a quote at the bottom of the edition page "Encyclopedic content must be verifiable." That seems clear. --
Somasimple (
talk)
05:06, 12 June 2010 (UTC)
From the Peak and Falling Phase" section:
However, the same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores; the sodium channels become inactivated. This lowers the membrane's permeability to sodium, driving the membrane voltage back down.
How? If some sodium is still flowing into the cell, the membrane voltage would continue to go up. Wouldn't it be the rate of increase that goes down?... And if the sodium flow is blocked completely, then how does this change the voltage at all? If the only thing driving down the voltage is the potassium outflow, then the last part of the quoted statement is misleading and needs to be fixed.
Thanks.
184.96.106.141 ( talk) 04:56, 12 January 2011 (UTC)
Let me leave a note that I'm going to try to do some serious work on this article. The main thing I've done so far is to move a bunch of material to the membrane potential article, so that this article doesn't repeat a lot of stuff that more properly belongs there. It needs instead to have a detailed discussion of voltage-gated ion channels and their effects on membrane potential. Looie496 ( talk) 19:17, 14 October 2011 (UTC)
Synaptidude ( talk) 07:57, 23 October 2011 (UTC)
So I would, maybe not so much as dispute that, but modify it a bit. I find it more useful to think of the relationship between voltage and channel opening in terms of probability. The actual functions that describe this relationship are exponentials or sums of exponentials, so they don't really have a distinct 'starting point'. Rather, they asymptote as they approach zero probability. So no, they really don't have a threshold or a precise voltage where they open. They have a precise probability for being open at a given voltage - and that's different because it's a smooth function without threshold. Even a voltage-gated sodium channel will open every now and aqain, even at a very hyperpolarized potential. As for the threshold of the action potential, it is determined only indirectly by the voltage-dependence of sodium channel opening. The single proximate basis of the AP threshold is the voltage where the sodium current becomes larger than the potassium current. This is, of course, influenced by how many sodium channels are open, but you can't ascribe the threshold solely to Na because it also depends on K. If you made a whole-cell current/voltage plot, you could pick out the threshold precisely as the voltage where the slope of the plot becomes negative. I tried to describe threshold this way (with a diagram) in an earlier version of this article, but it was clearly too technical for people's taste. Synaptidude ( talk) 01:24, 25 October 2011 (UTC)
...and just in case this horse is still breathing, even though precise, the probability function that describes the relationship between channel opening and voltage is not fixed. It depends on other things, such as the inactivation state of the channel. In the extreme case (and in a population of channels, since a single channel behaves stocastically) the probability of a channel in a population opening can be zero at all potentials, if they are all inactivated. So the probability that sodium channels will open at a given voltage depends on the history of the voltage, how long it's been since the voltage changed, etc. So basically, if you want to be accurate, you can't even say that the action potential threshold happens at a precise voltage, because that threshold is changing all the time because of the recent history of the membrane potential. Yes, if you hold the membrane at precisely the same potential for long enough for the channel to reach a steady state, then the threshold will be at the same place every time you test it. The only thing you can say with precision is that the action potential will fire at precisely the voltage where INa > IK - whatever the size of those currents are in a particular set of circumstances. Synaptidude ( talk) 05:12, 25 October 2011 (UTC)
...and sorry, but in all my verbosity, I forgot the main point I wanted to make. Because the threshold for the action potential is at the point where INa becomes larger than Ik, the sodium current can actually grow quite large before the threshold is reached. So even if you wanted to (incorrectly ;) say that sodium channel opening has a threshold, the threshold for the action potential occurs at some votage-distance from that 'threshold'. Obviously, the larger is Ik the farther along the voltage scale, and thus the farther from the sodium channel 'threshold', is the threshold for the AP. Thus, even if there was a true threshold for sodium channel opening, it is not directly related to the action potential threshold.
Now the question is, can we find a way to accurately describe the threshold without confusing everyone. Synaptidude ( talk) 05:28, 25 October 2011 (UTC)
I'd like to suggest a reorganization of this article to make it more readable and less repetitive. I'm prepared to do it over the next few weeks myself or with help, if there are no objections. In my eyes, there are 3 parts to this article, and most of my suggestions are for the 2nd.
1. The Lead/Overview - a lot of entries in the Talk agree this needs to be changed to be more coherent and accessible to the lay reader. I think we should make the 2nd paragraph of the lead a much shorter description, just the basic idea of what it means for an AP to be an AP (I know, harder than it sounds). The info currently in the 3rd paragraph should be later in the article - in it's place, we could put a paragraph that takes a quick introductory walk through the later sections. The Overview is okay, but I think voltage changes and threshold potential will make more sense if the explanation walks the reader through an image like Figure 1A, although one that is a little clearer. That is usually how the action potential is taught, with constant reference to a graph.
2. Current sections 2 through 6 - Here's where the article is a bit messy. How I think it could be organized:
I think Phases should be included in the Biophysical Basis section. Besides including a lot of similar information, the phases are described using the same mechanisms that are being talked about in 'Biophysics'. And the 'Biophysics' section currently has no structure - going through mechanisms phase-by-phase would give it that. The new section would have general information up front, then subsections for each phase.
The Neurotransmission section should be removed, and its contents sorted into the other sections. First of all, neurotransmission is about the release and reception of neurotransmitters - this is related to APs and should be referred to, but that can go in the 'Termination' section and be primarily links to relevant articles. Second, a lot of what's in this section rambles about things other than neurotransmission anyway. I'm not suggesting any particular content be removed, only moved. Some of that will be clear, some not - I don't know where the bit about sensory neurons and pacemaker potentials should go, though I do agree they should be in the article.
3. The miscellaneous sections - I have no issue with their organization.
So broadly speaking, the changes are to fix the beginning of the article for the lay reader, and then reorganize the middle sections so that they walk through the AP from how it starts, to how it moves, to what it does when it gets where it's going. ~ Twodarts ( talk) 02:21, 18 December 2011 (UTC)
The article states (emphasis mine):
First it says that the insulation prevents signal decay. Then it says that it's the gaps in the insulation that prevent signal decay (i.e., it's not the insulation itself), which implies to me that the insulation may even contribute to the decay (or why else would there be signal boosters needed?). Could someone do a bit of rewrite to clarify the intended meaning here? DMacks ( talk) 06:19, 12 January 2012 (UTC)
From what I understand, all-or-none signals should be digital. Unless I'm missing something here.-- Miracleman123 ( talk) 06:58, 4 July 2012 (UTC)
I popped in here because this article was in an error category (invalid LCCNs) and one thing I immediately noticed was that the references were /very/ messy. For one thing, only about half the books in the 'bibliography' section were actually cited, and there were a number of books that weren't in that section. I've been doing quite a bit of work on reorganizing how they are laid out, with the goal of trying to get them all into some kind of 'uniform' appearance, and laid out in a way that's actually useful.
Though I am changing the format of the book references to use |ref=harv, it's not out of any intention to violate CITEVAR, or force something like list-defined references on the article...the format as it existed was, like I said, very confused, and moving the books into a separate section and using {{ sfn}} and {{ sfnm}} seemed like the best way to hammer this into something more usable, and less messy.
I would ask, though, that if there is a problem with how I'm doing this, you just poke me and say 'hey dummy', do this instead... I'm not changing the content, but I think where I am now would be a better 'starting point' to get this to something decent that the regular content editors of this can deal with (and that's not ugly) than where it was, even if it means moving in a different direction. If anyone wants to comment, please do so... Revent talk 11:17, 27 August 2014 (UTC)
Is it accurate to understand that an action potential is what can happen at a place, position or point on a cell's membrane, as indicated or measured by a point probe, rather than the succession of AP along, say, a neuron's axon? That is, that an AP is not the traveling of an event (the "spike train"?), but just the occurrence of the voltage event at a point?
If so, could it be appropriate to amend and add to the first sentence in the intro, from, "In physiology, an action potential is a short-lasting event in which the electrical membrane potential of a cell rapidly rises and falls, following a consistent trajectory.",
to, "In physiology, an action potential is a short-lasting event at a position in a cell in which the electrical membrane potential rapidly rises and falls, following a consistent trajectory. An action potential at one position may initiate another following action potential in a nearby continuous part of the membrane, such that an impulse signal made up of a sequence of action potentials travels along the cell membrane." ? (Without the boldface used here to make the phrase stand out, and 'spike train & impulse struck out and signal replaced impulse.)
UnderEducatedGeezer (
talk)
03:53, 26 June 2016 (UTC)
Is a 'spike train' the succession of action potentials along axon (like a gunpowder fuse burning from start to finish along the length of the fuse), or a rapid repeated firing of the neuron itself (like a machine gun firing some number of rounds one after another rapidly from one trigger pull)? UnderEducatedGeezer ( talk) 04:00, 26 June 2016 (UTC)
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Recently a video explaining the action potential has been deleted (and it was the case for MANY medical articles on the same day). I do not know why it has been deleted but I am guessing that it was considered too "simple". I will not undo this deletion since I don't feel I'm entitled to but it does raise the question : are wikipedia article made for the people already in the medical field or for everyone ? If the answer is the former, it would be disappointing but I would understand the video deletion. If it's the latter... why has the video been removed? Simplification will always be made (even when expert talk to each other). I do not understand this choice that goes against a popular use of wikipedia. — Preceding unsigned comment added by Alouzi ( talk • contribs) 20:50, 16 April 2018 (UTC)
I have temporarily reverted a very large addition to the section on plant action potentials. For reference, here it is:
Extended content
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Plant action potentialsPlant and fungal cells [a] are also electrically excitable. The action potential observed in vascular plants is better observed than those of vegetative [1] [2] because the diffusion of electrical signals occurs primarily in the phloem sieve tube – a distinctive characteristic of higher plants [3]. [4] The general progression of plant action potentials is the same as animal action potentials, however, plants possess alternate mechanisms. Resting PhasePlant cells are commonly observed to have more negative resting membrane potentials and rising phase membrane potentials. For example, the Dionaea’s resting membrane potential is approximately -120mV [5], whereas neurons are regularly between -40mV to -90mV [6] . To attain understanding regarding plant action potentials, Opritov et al. recorded the electric potentials of maize leaves. To do so, they cut the leaf accordingly to allow aphids to attach for a long period to feed in efforts to expose the sieve. Once exposed, the researchers removed the aphids carefully with a laser to access the contents released by the leaf. This liquid-like substance was then measured with a microelectrode that was previously calibrated with a control of water. [7] The recorded values were similar to those that were expected when reviewing a study of Mimosa pudica [8] which indicated that the resting membrane potential measured was significant. Stimulation and Rising PhaseStimulation also induces action potentials within plant cells, the most commonly mentioned stimulation is touch [5]. Unlike animals, the plant’s action potentials will not register any information regarding the characteristics of the interaction. [2] Upon stimulation, the depolarization in plant cells is not accomplished by an uptake of positive sodium ions, but but rather the influx of calcium. [4] Logically, one can understand the plant’s lack of dependence on sodium ions to initiate depolarization because too many sodium ions lead to detrimental outcomes. [9] Together with the following release of positive potassium ions, which is common to plant and animal action potentials, the action potential in plants infers, therefore, an osmotic loss of salt (KCl), whereas the animal action potential is osmotically neutral, when equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells [b] indicates an osmotic function of electrical excitability in the common, unicellular ancestors of plants and animals under changing salinity conditions, whereas the present function of rapid signal transmission is seen as a younger accomplishment of metazoan cells in a more stable osmotic environment. [10] It must be assumed that the familiar signalling function of action potentials in some vascular plants (e.g. Mimosa pudica) arose independently from that in metazoan excitable cells. PeakAs calcium influxes towards the cytoplasm, they activate calcium-dependent anion channels, causing negatively charged ions, like chloride, to flow out of the cell; thus further depolarizing the membrane. Similarly to the resting membrane potentials of plants and animals, the peaks correspond in a similar manner: they are commonly more negative. Dionaea’s action potential usually maximizes at -20mV, approximately 60mV less than an average nerve cell. [3] Falling Phase and After-hyperpolarizationUnlike the rising phase and peak, the falling phase and after-hyperpolarization seem to depend primarily on cations that are not calcium. To initiate repolarization, the cell requires movement of potassium out of the cell through passive transportation on the membrane. This differs from neurons because the movement of potassium does not dominate the decrease in membrane potential; In fact, to fully repolarize, a plant cell requires energy in the form of ATP to assist in the release of hydrogen from the cell – utilizing a transporter commonly known as H+-ATPase. [7] [3] Refractory Period Although there is a lot of debate regarding the refractory period of a plant cell, what is not up to speculation is the fact that their refractory periods are much longer than those in animals, [8] and that in order to fire and action potential again, they require more sources for electrical current. [3] Although animals and plants both possess action potentials, those of plants are often overlooked or ignored due to the plants’ lack of nerves and nervous system. The deficiency of a brain or a specified location to integrate information makes it difficult to believe that action potentials of plants create a response; however, plants definitely do perceive stimuli (without information regarding it) that can develop into an (generic) effector response. [2]
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In part, there are formatting problems, but I also am concerned that this material fails WP:DUE. Plants just aren't that big a part of the topic, and it seems to me to be inappropriate to have so many subsections that recapitulate the descriptions of action potential stages higher on the page. -- Tryptofish ( talk) 22:33, 22 May 2018 (UTC)
The first sentence of the second paragraph is a bit wordy and confusing. I would suggest not mentioning saltatory conduction here. — Preceding unsigned comment added by Mikeyvon ( talk • contribs) 21:55, 16 September 2021 (UTC)
"In the Hodgkin–Huxley membrane capacitance model, the speed of transmission of an action potential was undefined and it was assumed that adjacent areas became depolarized due to released ion interference with neighbouring channels. Measurements of ion diffusion and radii have since shown this not to be possible.[citation needed]"
What is "ion interference" here? What radii are we talking about? And where are the citations? — Preceding
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The article is extremely confusing, there is a lot of material and definitions which are, however, poorly organized. A lot of repetitions and the flow of argument is completely absent. I'll see what i can do.
It is incredible that it is a FEATURED ARTICLE with so many problems
Rvfrolov (
talk)
18:32, 2 January 2009 (UTC) 2 January 2009
There are three articles now which discuss very much the same things with numerous repetitions and description of the same material in different terms.
As it was already suggested by Methoxyroxy 12:37, 2 November 2006 (UTC), it needs a really big clean-up and optimization. There is a lot of confusion there so I will do this albeit not at once. I will move different parts between these three articles, edit and unify their style etc. At later stage I will need someone who is native English speaker to do spellcheck. Rvfrolov ( talk) 20:52, 2 January 2009 (UTC)
The current version of the article mixes action potentials with propagation of potentials creating excessive complexity and inaccuracies.
Potential propagation is not a required property of an action potential. Most textbooks first define the action potential in an isopotential cell. In Hodkin and Huxley's experiments, for example, a wire was strung along a squid giant axon to shunt axial currents effectively producing an isopotential membrane compartment. With this preparation, current-clamp experiments still produce action potentials along the entire fiber, without a "wave of electrochemical activity." Neither does a cell need to carry APs over a distance to make use of action potentials (e.g. electrocyte action potentials in electric fish, and many other cell types produce action potentials for other reasons than long-distance signaling).
The current definition is also missing a key defining component: the key role of voltage-sensitive conductances.
Propagating action potentials may be more consistently described as a continuous succession of local action potentials triggering action potentials in the adjacent sections. This distinction would help avoid some of the current inaccuracies in the article.
For example, the current article describes saltatory conduction as follows "Since the axon is insulated, the action potential can travel through it without significant signal decay." In reality, myelinated stretches of axons do not produce action potentials and the action potential does not "travel through it." It would be more accurate to state that depolarization from an action potential at one node propagates passively to the next node and triggers an action potential at the next node. The signal may decay significantly between nodes and still trigger an action potential at the next node. The same section seems to imply that the action potential must be generated at the synapse for the release of neurotransmitter, which is also inaccurate. Any depolarization of sufficient magnitude (passive or active) will have a similar effect.
In summary, to make the article more useful, I recommend providing a complete and general definition of the action potential with minimal extraneous detail. The adjacent topics such as "Electrotonic propagation of potentials", "Neurotransmitter release", "Cable theory", "Saltatory conduction", probably belong in separate articles or sections.
Yatsenko DV ( talk) 03:45, 27 July 2009 (UTC)
I am removing "nerve spikes" from the first sentence.
I do not believe that the term "nerve spike" could be generally applied to all action potentials. Action potentials are transient membrane voltage events in individual cells or their compartments. They happen in many cell types. Nerves are bundles of axons in the peripheral nervous system (no nerves in the brain or spinal cord). Thus "nerve spikes" are but one specific manifestation of action potentials. The same could be said about MUAPs (motor unit action potentials), for example. This does not make them synonymous with action potentials. Dimitri Yatsenko 01:25, 28 July 2009 (UTC)
The current wording in the second paragraph states that depolarization "increases both the inward sodium current (depolarization) and the balancing outward potassium current (repolarization/hyperpolarization)". I question the accuracy of that statement.
As the membrane depolarizes, the membrane potential moves toward the reversal potential for sodium. This reduces the electrochemical driving force for sodium. Unless the sodium conductance increases by a greater factor to compensate, the sodium current will decrease, not increase. So the statement is not generally accurate. I propose rewording it to state that both conductances increase and only when the net current is negative and leads to further depolarization, a positive feedback loop is generated to precipitate the action potential. Dimitri Yatsenko 21:07, 28 July 2009 (UTC) —Preceding unsigned comment added by Yatsenko DV ( talk • contribs)
In the "Quantitative models" section there are many references to things being simple or a simplification. While this section does have many references attached to it, there is no mention in the article of what these things are simpler than. That is, why are these things simple, and compared to what, and what would be more complex.
The refractory period section seems like it was copy pasted from a text book which was written by a high school teach held at gun point. Perhaps we should consider updating it Paskari ( talk) 23:30, 6 October 2009 (UTC)
I've just attempted a pretty major rewrite of the lead, which I hope won't offend anybody. I thought the existing version was too hard for readers to understand -- it also contained a couple of minor errors. I also added a paragraph about the distinction between sodium and calcium spikes, which seems to me to be a very important point. Regards, Looie496 ( talk) 20:08, 23 February 2010 (UTC)
I have removed a reference from the lede that was to:
{{
cite book}}
: CS1 maint: multiple names: authors list (
link)Alphascript Publishing republished Wikipedia content. And the book in question republishes this article. The cover of the book can be seen [http://www.amazon.com/Cardiac-action-potential-Frederic-Miller/dp/6130098685/ref=sr_1_1?ie=UTF8&s=books&qid=1267362547&sr=1-1 on Amazon]. This article is named on the front cover. (The format for Alphascript books is to list the WP articles contained therein on the front cover as part of the name.)
The person who owns the book can verify that this is republished Wikipedia content by looking at the copyright information inside the book itself. -- RA ( talk) 13:16, 28 February 2010 (UTC)
The region with high concentration will diffuse out toward the region with low concentration. To extend the example, let solution A have 30 sodium ions and 30 chloride ions. Also, let solution B have only 20 sodium ions and 20 chloride ions. Assuming the barrier allows both types of ions to travel through it, then a steady state will be reached whereby both solutions have 25 sodium ions and 25 chloride ions. If, however, the porous barrier is selective to which ions are let through, then diffusion alone will not determine the resulting solution. Returning to the previous example, let's now construct a barrier that is permeable only to sodium ions. Since solution B has a lower concentration of both sodium and chloride, the barrier will attract both ions from solution A.
There is not a single citation about osmosis. Osmosis tells us exactly the contrary. Facts tells us the same thing as osmosis: The cited diffusion doesn't occur. The concentrations may be equilibrated by water movement and membrane is permeable to water through aquaporins or directly. Somasimple ( talk) 05:28, 3 June 2010 (UTC)
Secondly,
If solution A is electroneutral THEN 30n+30p=0 (where n stands for negative and p for positive). If solution B is also electroneutral THEN 25n+25p=0. Considering an action from a compartment onto another one orders to consider all positive and negative charges that exist in the compartments.
So, there is NO electric flux OR electric field BECAUSE EACH compartment is neutral at start. Saying a compartment is neutral is saying that it can't exert any electric "thing" at all.
Conclusion: You can't get something that is the result of k(25p/30p) or k(30p/25p). That is mathematically and physically incorrect because you arbitrarily remove the negative charges without any scientific explanation. Somasimple ( talk) 09:27, 3 June 2010 (UTC)
The inward movement of sodium ions and the outward movement of potassium ions are passive
Let's describe all the events that happen simultaneously:
1/ Sodium movement balanced with chloride
sodium is inward and Na ions stick to the internal membrane, chloride ions stay out, and balance the Na charge, across the external membrane
2/ Potassium movement balanced with chloride
potassium is outward and K ions stick to the external membrane, chloride ions stay in, and balance the K charge, across the internal membrane
Now let's see what happens on each side:
1/ Internal side:
sodium is inward and Na ions stick to the internal membrane, chloride ions stay in, and balance the K charge, across the internal membrane
2/ External side
chloride ions stay out, and balance the Na charge, across the external membrane, potassium is outward and K ions stick to the external membrane
Result: a membrane voltage that is... quite null.
Osmosis: Since there are concentrations changes there is water flux through aquaporins:
1/ from int to ext for sodium
2/ from ext to int for potassium
Result : How is it possible to make a bidirectional and simultaneous water movement in aquaporins? Somasimple ( talk) 05:57, 5 June 2010 (UTC)
About this section Myelin and saltatory conduction It is said:
The first assertion is false since every axon is covered by myelin; compact or not, leaving no room (<20 nm) around the axon. See the excellent book, page 128 [http://www.amazon.com/Neurocytology-Structure-Neurons-Processes-Neuroglial/dp/313781801X/ref=sr_1_1?ie=UTF8&s=books&qid=1276061846&sr=1-1 Neurocytology: Fine Structure of Neurons, Nerve Processes and Neuroglial Cells]
The second becomes, in that case, not true since it assumes that unmyelinated axons are bare. -- Somasimple ( talk) 05:43, 9 June 2010 (UTC)
In this article [
Cable Theory] the conduction velocity depends greatly of the time constant that is result of τm=Cm*Rm
It is said that myelin decreases the membrance capacitance. That's seems OK but what happens to the membrane resistance in case of myelinization?
Computation of the the time constant with reasonable values leads to an increase of the time constant:
You may see a
discussion about this problem.--
Somasimple (
talk)
10:55, 11 June 2010 (UTC)
![]() | This page is not a forum for general discussion about Action potential. Any such comments may be removed or refactored. Please limit discussion to improvement of this article. You may wish to ask factual questions about Action potential at the Reference desk. |
-- Tryptofish ( talk) 19:21, 11 June 2010 (UTC)
Everyone know this limitation. Does that mean that errors must NOT be discussed and thus articles, NOT improved?
I brought in the previous section a computation that contradicts the notion of velocity improvement by capacitance reduction of myelin. You get any rigth to bring another computation that tells something else or you MUST accept the fact that article formulation is wrong even if it contradicts your actual conviction. Here is a quote at the bottom of the edition page "Encyclopedic content must be verifiable." That seems clear. --
Somasimple (
talk)
05:06, 12 June 2010 (UTC)
From the Peak and Falling Phase" section:
However, the same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores; the sodium channels become inactivated. This lowers the membrane's permeability to sodium, driving the membrane voltage back down.
How? If some sodium is still flowing into the cell, the membrane voltage would continue to go up. Wouldn't it be the rate of increase that goes down?... And if the sodium flow is blocked completely, then how does this change the voltage at all? If the only thing driving down the voltage is the potassium outflow, then the last part of the quoted statement is misleading and needs to be fixed.
Thanks.
184.96.106.141 ( talk) 04:56, 12 January 2011 (UTC)
Let me leave a note that I'm going to try to do some serious work on this article. The main thing I've done so far is to move a bunch of material to the membrane potential article, so that this article doesn't repeat a lot of stuff that more properly belongs there. It needs instead to have a detailed discussion of voltage-gated ion channels and their effects on membrane potential. Looie496 ( talk) 19:17, 14 October 2011 (UTC)
Synaptidude ( talk) 07:57, 23 October 2011 (UTC)
So I would, maybe not so much as dispute that, but modify it a bit. I find it more useful to think of the relationship between voltage and channel opening in terms of probability. The actual functions that describe this relationship are exponentials or sums of exponentials, so they don't really have a distinct 'starting point'. Rather, they asymptote as they approach zero probability. So no, they really don't have a threshold or a precise voltage where they open. They have a precise probability for being open at a given voltage - and that's different because it's a smooth function without threshold. Even a voltage-gated sodium channel will open every now and aqain, even at a very hyperpolarized potential. As for the threshold of the action potential, it is determined only indirectly by the voltage-dependence of sodium channel opening. The single proximate basis of the AP threshold is the voltage where the sodium current becomes larger than the potassium current. This is, of course, influenced by how many sodium channels are open, but you can't ascribe the threshold solely to Na because it also depends on K. If you made a whole-cell current/voltage plot, you could pick out the threshold precisely as the voltage where the slope of the plot becomes negative. I tried to describe threshold this way (with a diagram) in an earlier version of this article, but it was clearly too technical for people's taste. Synaptidude ( talk) 01:24, 25 October 2011 (UTC)
...and just in case this horse is still breathing, even though precise, the probability function that describes the relationship between channel opening and voltage is not fixed. It depends on other things, such as the inactivation state of the channel. In the extreme case (and in a population of channels, since a single channel behaves stocastically) the probability of a channel in a population opening can be zero at all potentials, if they are all inactivated. So the probability that sodium channels will open at a given voltage depends on the history of the voltage, how long it's been since the voltage changed, etc. So basically, if you want to be accurate, you can't even say that the action potential threshold happens at a precise voltage, because that threshold is changing all the time because of the recent history of the membrane potential. Yes, if you hold the membrane at precisely the same potential for long enough for the channel to reach a steady state, then the threshold will be at the same place every time you test it. The only thing you can say with precision is that the action potential will fire at precisely the voltage where INa > IK - whatever the size of those currents are in a particular set of circumstances. Synaptidude ( talk) 05:12, 25 October 2011 (UTC)
...and sorry, but in all my verbosity, I forgot the main point I wanted to make. Because the threshold for the action potential is at the point where INa becomes larger than Ik, the sodium current can actually grow quite large before the threshold is reached. So even if you wanted to (incorrectly ;) say that sodium channel opening has a threshold, the threshold for the action potential occurs at some votage-distance from that 'threshold'. Obviously, the larger is Ik the farther along the voltage scale, and thus the farther from the sodium channel 'threshold', is the threshold for the AP. Thus, even if there was a true threshold for sodium channel opening, it is not directly related to the action potential threshold.
Now the question is, can we find a way to accurately describe the threshold without confusing everyone. Synaptidude ( talk) 05:28, 25 October 2011 (UTC)
I'd like to suggest a reorganization of this article to make it more readable and less repetitive. I'm prepared to do it over the next few weeks myself or with help, if there are no objections. In my eyes, there are 3 parts to this article, and most of my suggestions are for the 2nd.
1. The Lead/Overview - a lot of entries in the Talk agree this needs to be changed to be more coherent and accessible to the lay reader. I think we should make the 2nd paragraph of the lead a much shorter description, just the basic idea of what it means for an AP to be an AP (I know, harder than it sounds). The info currently in the 3rd paragraph should be later in the article - in it's place, we could put a paragraph that takes a quick introductory walk through the later sections. The Overview is okay, but I think voltage changes and threshold potential will make more sense if the explanation walks the reader through an image like Figure 1A, although one that is a little clearer. That is usually how the action potential is taught, with constant reference to a graph.
2. Current sections 2 through 6 - Here's where the article is a bit messy. How I think it could be organized:
I think Phases should be included in the Biophysical Basis section. Besides including a lot of similar information, the phases are described using the same mechanisms that are being talked about in 'Biophysics'. And the 'Biophysics' section currently has no structure - going through mechanisms phase-by-phase would give it that. The new section would have general information up front, then subsections for each phase.
The Neurotransmission section should be removed, and its contents sorted into the other sections. First of all, neurotransmission is about the release and reception of neurotransmitters - this is related to APs and should be referred to, but that can go in the 'Termination' section and be primarily links to relevant articles. Second, a lot of what's in this section rambles about things other than neurotransmission anyway. I'm not suggesting any particular content be removed, only moved. Some of that will be clear, some not - I don't know where the bit about sensory neurons and pacemaker potentials should go, though I do agree they should be in the article.
3. The miscellaneous sections - I have no issue with their organization.
So broadly speaking, the changes are to fix the beginning of the article for the lay reader, and then reorganize the middle sections so that they walk through the AP from how it starts, to how it moves, to what it does when it gets where it's going. ~ Twodarts ( talk) 02:21, 18 December 2011 (UTC)
The article states (emphasis mine):
First it says that the insulation prevents signal decay. Then it says that it's the gaps in the insulation that prevent signal decay (i.e., it's not the insulation itself), which implies to me that the insulation may even contribute to the decay (or why else would there be signal boosters needed?). Could someone do a bit of rewrite to clarify the intended meaning here? DMacks ( talk) 06:19, 12 January 2012 (UTC)
From what I understand, all-or-none signals should be digital. Unless I'm missing something here.-- Miracleman123 ( talk) 06:58, 4 July 2012 (UTC)
I popped in here because this article was in an error category (invalid LCCNs) and one thing I immediately noticed was that the references were /very/ messy. For one thing, only about half the books in the 'bibliography' section were actually cited, and there were a number of books that weren't in that section. I've been doing quite a bit of work on reorganizing how they are laid out, with the goal of trying to get them all into some kind of 'uniform' appearance, and laid out in a way that's actually useful.
Though I am changing the format of the book references to use |ref=harv, it's not out of any intention to violate CITEVAR, or force something like list-defined references on the article...the format as it existed was, like I said, very confused, and moving the books into a separate section and using {{ sfn}} and {{ sfnm}} seemed like the best way to hammer this into something more usable, and less messy.
I would ask, though, that if there is a problem with how I'm doing this, you just poke me and say 'hey dummy', do this instead... I'm not changing the content, but I think where I am now would be a better 'starting point' to get this to something decent that the regular content editors of this can deal with (and that's not ugly) than where it was, even if it means moving in a different direction. If anyone wants to comment, please do so... Revent talk 11:17, 27 August 2014 (UTC)
Is it accurate to understand that an action potential is what can happen at a place, position or point on a cell's membrane, as indicated or measured by a point probe, rather than the succession of AP along, say, a neuron's axon? That is, that an AP is not the traveling of an event (the "spike train"?), but just the occurrence of the voltage event at a point?
If so, could it be appropriate to amend and add to the first sentence in the intro, from, "In physiology, an action potential is a short-lasting event in which the electrical membrane potential of a cell rapidly rises and falls, following a consistent trajectory.",
to, "In physiology, an action potential is a short-lasting event at a position in a cell in which the electrical membrane potential rapidly rises and falls, following a consistent trajectory. An action potential at one position may initiate another following action potential in a nearby continuous part of the membrane, such that an impulse signal made up of a sequence of action potentials travels along the cell membrane." ? (Without the boldface used here to make the phrase stand out, and 'spike train & impulse struck out and signal replaced impulse.)
UnderEducatedGeezer (
talk)
03:53, 26 June 2016 (UTC)
Is a 'spike train' the succession of action potentials along axon (like a gunpowder fuse burning from start to finish along the length of the fuse), or a rapid repeated firing of the neuron itself (like a machine gun firing some number of rounds one after another rapidly from one trigger pull)? UnderEducatedGeezer ( talk) 04:00, 26 June 2016 (UTC)
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Recently a video explaining the action potential has been deleted (and it was the case for MANY medical articles on the same day). I do not know why it has been deleted but I am guessing that it was considered too "simple". I will not undo this deletion since I don't feel I'm entitled to but it does raise the question : are wikipedia article made for the people already in the medical field or for everyone ? If the answer is the former, it would be disappointing but I would understand the video deletion. If it's the latter... why has the video been removed? Simplification will always be made (even when expert talk to each other). I do not understand this choice that goes against a popular use of wikipedia. — Preceding unsigned comment added by Alouzi ( talk • contribs) 20:50, 16 April 2018 (UTC)
I have temporarily reverted a very large addition to the section on plant action potentials. For reference, here it is:
Extended content
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Plant action potentialsPlant and fungal cells [a] are also electrically excitable. The action potential observed in vascular plants is better observed than those of vegetative [1] [2] because the diffusion of electrical signals occurs primarily in the phloem sieve tube – a distinctive characteristic of higher plants [3]. [4] The general progression of plant action potentials is the same as animal action potentials, however, plants possess alternate mechanisms. Resting PhasePlant cells are commonly observed to have more negative resting membrane potentials and rising phase membrane potentials. For example, the Dionaea’s resting membrane potential is approximately -120mV [5], whereas neurons are regularly between -40mV to -90mV [6] . To attain understanding regarding plant action potentials, Opritov et al. recorded the electric potentials of maize leaves. To do so, they cut the leaf accordingly to allow aphids to attach for a long period to feed in efforts to expose the sieve. Once exposed, the researchers removed the aphids carefully with a laser to access the contents released by the leaf. This liquid-like substance was then measured with a microelectrode that was previously calibrated with a control of water. [7] The recorded values were similar to those that were expected when reviewing a study of Mimosa pudica [8] which indicated that the resting membrane potential measured was significant. Stimulation and Rising PhaseStimulation also induces action potentials within plant cells, the most commonly mentioned stimulation is touch [5]. Unlike animals, the plant’s action potentials will not register any information regarding the characteristics of the interaction. [2] Upon stimulation, the depolarization in plant cells is not accomplished by an uptake of positive sodium ions, but but rather the influx of calcium. [4] Logically, one can understand the plant’s lack of dependence on sodium ions to initiate depolarization because too many sodium ions lead to detrimental outcomes. [9] Together with the following release of positive potassium ions, which is common to plant and animal action potentials, the action potential in plants infers, therefore, an osmotic loss of salt (KCl), whereas the animal action potential is osmotically neutral, when equal amounts of entering sodium and leaving potassium cancel each other osmotically. The interaction of electrical and osmotic relations in plant cells [b] indicates an osmotic function of electrical excitability in the common, unicellular ancestors of plants and animals under changing salinity conditions, whereas the present function of rapid signal transmission is seen as a younger accomplishment of metazoan cells in a more stable osmotic environment. [10] It must be assumed that the familiar signalling function of action potentials in some vascular plants (e.g. Mimosa pudica) arose independently from that in metazoan excitable cells. PeakAs calcium influxes towards the cytoplasm, they activate calcium-dependent anion channels, causing negatively charged ions, like chloride, to flow out of the cell; thus further depolarizing the membrane. Similarly to the resting membrane potentials of plants and animals, the peaks correspond in a similar manner: they are commonly more negative. Dionaea’s action potential usually maximizes at -20mV, approximately 60mV less than an average nerve cell. [3] Falling Phase and After-hyperpolarizationUnlike the rising phase and peak, the falling phase and after-hyperpolarization seem to depend primarily on cations that are not calcium. To initiate repolarization, the cell requires movement of potassium out of the cell through passive transportation on the membrane. This differs from neurons because the movement of potassium does not dominate the decrease in membrane potential; In fact, to fully repolarize, a plant cell requires energy in the form of ATP to assist in the release of hydrogen from the cell – utilizing a transporter commonly known as H+-ATPase. [7] [3] Refractory Period Although there is a lot of debate regarding the refractory period of a plant cell, what is not up to speculation is the fact that their refractory periods are much longer than those in animals, [8] and that in order to fire and action potential again, they require more sources for electrical current. [3] Although animals and plants both possess action potentials, those of plants are often overlooked or ignored due to the plants’ lack of nerves and nervous system. The deficiency of a brain or a specified location to integrate information makes it difficult to believe that action potentials of plants create a response; however, plants definitely do perceive stimuli (without information regarding it) that can develop into an (generic) effector response. [2]
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In part, there are formatting problems, but I also am concerned that this material fails WP:DUE. Plants just aren't that big a part of the topic, and it seems to me to be inappropriate to have so many subsections that recapitulate the descriptions of action potential stages higher on the page. -- Tryptofish ( talk) 22:33, 22 May 2018 (UTC)
The first sentence of the second paragraph is a bit wordy and confusing. I would suggest not mentioning saltatory conduction here. — Preceding unsigned comment added by Mikeyvon ( talk • contribs) 21:55, 16 September 2021 (UTC)
"In the Hodgkin–Huxley membrane capacitance model, the speed of transmission of an action potential was undefined and it was assumed that adjacent areas became depolarized due to released ion interference with neighbouring channels. Measurements of ion diffusion and radii have since shown this not to be possible.[citation needed]"
What is "ion interference" here? What radii are we talking about? And where are the citations? — Preceding
unsigned comment added by
89.3.212.183 (
talk)
02:20, 3 July 2022 (UTC)
Cite error: There are <ref group=lower-alpha>
tags or {{efn}}
templates on this page, but the references will not show without a {{reflist|group=lower-alpha}}
template or {{notelist}}
template (see the
help page).