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Why does an active potential create an electric impulse?

  1. Jan 6, 2010 #1
    I read about it but I don't get it. I can understand how current would flow if one side is positive and other negative but I don't understand what is happening in an axon


    I don't understand how current is flowing is it flowing vertically?. What is this electric impulse? Also since at resting potential there is a difference of voltage. Why doesn't this cause electrical impulse. Please help. Thanks :smile:
  2. jcsd
  3. Jan 6, 2010 #2
    I'm having difficulties understanding exactly what your question is. So I'm wondering:
    Do you know about the ion pumps for sodium/potassium?
    Do you know what IPSP and EPSP are?

    You should look into more information on the axon hillock.
    I believe it will help you in your understanding but I'm not exactly sure since I don't understand what you are asking. If you still need help with the specifics on something then ask away or you can just send me a PM.
  4. Jan 6, 2010 #3
    i don't believe there is actual current flow when one side is positive and the other negative(wrt). there is a potential difference because ion pumps create an imbalance of charge across the membrane. then, when channels open in the membrane, there is a flow of charge across the membrane and the membrane depolarizes.
  5. Jan 6, 2010 #4
    I understand ion pumps. I don't understand exactly what is happening here. I'm assuming this is like a wire conducting electricty. Where postitive ions flow from negative to positive. Now looking back I think I'm wrong. So what happens. This is my new understanding please tell me if this is right.

    1. When they say voltage travels across the axon what to they mean?
    Do they mean that required ion channels open or close creating depolarization inside the membrane. Is is it the gradual increase of depolarization that makes the voltage travel across.
    2. What to they mean when an action potential is fired?
    3. How is neurotransmitter released as an action potential?
    How does it know depolarization has occured.
    4. Why hyperpolarization doesn't create much action potential?
    5. In the resting potential -70mv there is still a voltage difference?
    Why are ion channels not open at this stage. Is this the norm and ion channels are not designed to open at this potential
    6. Apart from neurotranmitter ions can also be released. How does this occur?

    Thanks a lot!!
  6. Jan 8, 2010 #5


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    Really? What is the law that permits positive ions (or negative) to flow in a direction?
    Coulomb's law says only that a charge may exert a force that depends from this charge. BTW, solutes are expected to be neutral...
  7. Jan 8, 2010 #6
    Well, the first thing is to stop thinking of it as current. current flows over a wire much the same way water flows through a pipe. Conceptually an action potential is more like a set of dominos falling over one by one.

    Consider the following membrane:


    At rest, the ion pumps preserve the potential difference across the membrane in a stable configuration. As the action potential is triggered, the first domino topples:


    This destabilizes the membrane locally, causing adjoining ionic gates to open. As these gates allow in ions, the ion pumps go to work to reestablish the membrane potential (represented below by | ):




    The action of the ionic pump is very important in understanding AP's, as it not only restabilizes the membrane, but it also prevents back-propagation of a potential, since it is just a bit slower than the destabilization mechanism.

    Once the AP reaches the axon hillock, it is the destabilization of the membrane that triggers release of neurotransmitters. The specific mechanisms differ from one NT to another, but the general idea is the same.

    Now, for extra credit, see if you can figure out why myelinated nerves can transmit an AP much faster than nonmyelinated nerves.
  8. Jan 8, 2010 #7
    Hmmm I would rather say than voltage travelling accross the axon as electrical impulse o nerve impulse travels accross the membrane. The way this works is by the ion pumps allowing depolarization to cross the threshold of the cell. For most cells this is somewhere around -55mV (resting potential is around -70mV). These numbers change depending on the cell and how long since the cell was last active. If a cell had just fired it can not fire again and it is in a period of rest... after this period of rest it will require a higher membrane potential in order for an action potential to be started. What an action potential MEANS is that the cell is in a positive feedback situation where the flow of na ions continues to increase quite quickly.

    2. An action potential is fired when the threshold for that cell is crossed and the cell enters a positive feedback situation. The positive feedback situation is just to say that the flow of na/k ions is unstable in an ever more increasing fashion. So this causes the membrane potential to go up fast until the peak at approximately 35mV.

    3. Neurotransmitters are not released as 'action potentials'. Neurotransmitters are created in the cell and store in synaptic vessicles in an axon terminal. They are stored there until an AP reaches the terminal which causes the Ca pumps to flow ions into the axon which in turn directs the synaptic vessicles to leave the axon and deposit their neurotransmitters into the synaptic cleft. These neurotransmitters are received by the dendrite of the next cell and have either ESPS or ISPS properties. That is either they excite or inhibit the cell. They do this by changing the cells permeability to ions. The neurotransmitters are either destroyed or returned to the cell they originated from to be reused.

    4. I'm not sure exactly what you mean by 'knows' but I'll just say that depolarization is controlled by the biochemistry. So nothing really 'knows' what's going on it just happens based on the chemistry and physics of the situation.

    5. Hyperpolarization is the opposite of an action potential. It is just a way to describe the membrane potential going more negative than rest.

    6. The membrane potential is just the difference of voltage between the inside of the cell and the outside. This is maintained by the ion pumps and is there pretty much because it 'has' to be. These differences in voltage... or concentration of ions... are what allow the cells to function.

    7. Hmm well, ion channels are open and they are called K leak channels (potassium leak channels) they allow potassium ions to flow pretty much the same way they would flow in water. That is they do not require extra energy to flow they flow on a gradient.

    8. I'm not sure what exactly you want from this question. I'll give an example of something I'm more familiar with though and see if it's what your talking about:

    As an action potential travels down a cell it can reach somethign called a DHP receptor. When this is activated it causes a ryanodine channel to be opened which causes a release of Ca ions. These ions attach themselves to troponin on an actin filament. This causes the unwinding of tropomyosin to expose actin active sites. Myosin can then bind to the actin filament and 'pull' it producing force. This is how our muslces work.
  9. Jan 9, 2010 #8
  10. Jan 10, 2010 #9
    Thanks for all the wonderful answers. Thanks especially for sorry, karma and protein soup.
    So is the purpose of an active potential is to open calcium channels so they bind to neurotransmitter. So why can't they just send a chemical to do that. Why do they need active potentials? Is it simply the way body was made. Also for cardiac function automatic action potential are required, is that the reason this is created this way? Also let's say I want to flex my finger a little bit. How does this happen? Does the frequency of the signal alters so there is weak contraction, how does the action potential finally cease? How does the cell know it has to pass inhibitory neurotransmitters at the right time?

    Can the amount of neurotransmitters transferred affect the rate at action potential is reached?As the action potential frequency in a presynaptic neuron increases the number of vesicles undergoing exocytosis and the number of released neurotransmitter molecules increases or not?I think it only affects the rate, am I right? Also if some cell has leaky Calcium channels does that mean it would activate neurotransmitter and send signals?

    Thank you!!
    Last edited: Jan 10, 2010
  11. Jan 10, 2010 #10
    These are all great questions I've gotta run right at this moment but I'm sure someone else will respond with answers and if not later when I come back I will respond myself :smile:
  12. Jan 10, 2010 #11
    OK I am back home and have a few moments to spare to answer some of your questions.

    Firstly the 'purpose' of an action potential is more of a getting a signal from point a to point b, and the way it travels in our body is through nerve impulses. The action potential is one part of the impulses journey but action potentials do not always have to be associated with the release of neurotransmitters. Release of neurotransmitters are just another part of sending on the 'message'.

    As well action potentials do work on a chemical basis, that's what makes them work. I think the reason that axons are used to transmit these electro-chemical signals has to do with speed and the fact it enables a 'direct' connection to various parts of the body. I.e. if the body were to just release a chemical from your brain to tell you to move your foot it would probably take quite some time before your foot moves because the chemical has no direct connection and has to travel through your body using other mechanisms. I'm not 100% sure on this however so anyone can feel free to jump in.

    Yes the cardiac system is built with something called cardiac muscle automaticity. This is so the heart can keep a steady rhythm notably occuring from the SA node. If your heart begins to lose automaticity it is detected by a change in heart rhythm and is the cause of cardiac rest etc. I'm pretty sure not all organisms have this automaticity which is regulated by a specific node but rather work by each cell knowing the rhythm. Human cardiac cells can work independently in this fashion too even if they are removed from the heart but in order to make sure automaticity and give greater control over the cardiac system the SA node is put into place.

    In my previous post I showed how a muscle would be contracted after an action potential is received from the motor neurons. (Contraction when speaking about the muscular system refers to muscle fibres generating tension not specific of shortening or lengthening of the muscle itself) The length of contraction and strength of the contraction all depends on how many muscle cells are being used and for how long. The way that the muscle stops contraction is the opposite of how it began, calcium moves back to the sarcoplasm reticulum. The calcium molecules then have to unbind from the tropomin in order to maintain the ion concentration in the reticulum. This means that tropomyosin can bind back into regular position blocking the binding sites not. The way this all begins is from your CNS and it is controlled by your CNS. I'm not exactly how YOU personally control it though, it's always been a great mystery to me. How when you 'think, move my arm' your arm moves.

    anyways thats all the time I have for now, I'll try to clear up some things later :smile: Hope this information helps you.
  13. Jan 10, 2010 #12
    Thanks a lot for taking your time to answer my questions "sorry!". Your answers have been certainly been very helpful :smile: Yeah I think you are right if we send a chemical it might take forever for the signal to reach. I understood how the muscle contraction cease by your explanation, but isn't the active potential still there. Wouldn't it come back and activate the muscle cell, how is the active potential ceased?
    Also a new question normal cardiac muscle cell do not have automacity right, only nodes have it right?

    These are the questions remaining

    "Does the frequency of the signal alters so there is weak contraction, how does the action potential finally cease? How does the cell know it has to pass inhibitory neurotransmitters at the right time?Can the amount of neurotransmitters transferred affect the rate at action potential is reached?As the action potential frequency in a presynaptic neuron increases the number of vesicles undergoing exocytosis and the number of released neurotransmitter molecules increases or not?I think it only affects the rate, am I right? Also if some cell has leaky Calcium channels does that mean it would activate neurotransmitter and send signals?"

    Again thanks a lot for your time :smile:
    Last edited: Jan 10, 2010
  14. Jan 11, 2010 #13
    Hey no problem that's what the site is for right?

    The action potential isn't actually a 'thing' that travels around, it's more of a phase that a 'special' cell membrane goes through to transmit a nerual impulse, such as in an axon. So once the impulse is transmitted through that particular cell the action potential is over and the cell membrane returns to resting potential after a brief 'undershoot'. So nothing really 'ceases' the action potential in a particular cell, it's just a phase that pases by in the transmission of an impulse.

    Now you must recall that the way that this works is that the action potential travels through to the axon terminal which releases neurotransmitters to excite or inhibit the next. For most motor neurons the excitory neurotransmitter is acetylcholine, stop this or use another molecule which will inhibit that particular neuron and you stop the contraction for that particular muscle fibre. So when a muscle contracts it has received a signal from a motor neuron to do so. It will continue to contract until Ca ions have returned to "normal" in the sarcoplasm. It's important to understand that during a muscle contraction you are not using all your muscle fibres, you are only recruiting the amount needed depending on how long and how strong the contraction is/has been going on for.
    This might be confusing to you sorry, it's just hard for me to explain.

    Now on to your other questions :smile:

    The frequency of signal doesn't change but the amount of muscle fibres being recruited does. Low strength=low muscle fibres and vice versa. It is stopped once your CNS stops sending these signals and in some cases instead releases molecules for inhibition for muscle contraction (which in the case of you flexing your finger is more than likely controlled by your brain.)

    The way neurotransmitters work is more in 'stages' the reason being is because sometimes one vessicle will occasionally leave the presynaptic cell. The body is set up so that these will not cause action potentials. This article discusses releasing ESPSs to achieve action potentials: http://en.wikipedia.org/wiki/Excitatory_postsynaptic_potential.

    I think that I've answered those remaining questions from before if I missed anything or something isn't clear just holla :tongue:. Sorry that it took me so long to type the rest of this up I was kind of busy today.

    Things I think are important to understand with regard to action potentials and neurons etc.:
    -Action potentials are a phase which an excitable membrane go through after the membrane potential reaches the threshold voltage.
    -After action potentials occur a excitable membrane does not transmit again and again right away, the membrane goes through a period of rest and after this rest period it requires more of a voltage difference for it to be excited.
    -Neurotransmission occurs in stages, this is important to understand with regard to your 'leaky' calcium question. However if this occured severly as to release more and more neurotransmitters I am not sure how it would effect the area or what the bodies response to this would be.
    -One motor neuron controls only one area of muscle fibre, they are recruited in sync to change the strength of contraction.
    -Muscle contraction stops by inhibition of motor neurons so either the excited neurons are inhibited and the resting cells do not receive any excitory neurotransmitters.

    EDIT: I just realized I had forgotten about your question with regard to cardiac muscle. Cardiac autmaticity means that cardiac cells are able to operate on their own independent of an outside impulse. They basically create their own impulse and start an action potential on their own. The SA and AV nodes have these cells but the normal cardiac cells all have the capability. The SA node has a higher automaticity than the rest however and that is why it is responsible for heart rate. However sometimes other cardiac cells do fire off and this is this is known as ectopic focus, the cause of this however is pathological, so it is not normal for cardiac cells to do this. It normally does not cause any problem but it can cause cardiac dysrhythmia, or abnormal rhythm of the heart beat. If this occurs frequently it can cause poor cardiac contractions and thus reduce the hearts ability to pump blood.
    As well I'm interested if this is just for personal knowledge or for a course, if it's for a course it would be helpful if I knew what level you are studying at. I'm all for having greater knowledge over things that interest you but if this is for a course you should focus mostly on understanding what is required before venturing out into other areas. So just make sure you understand what you need to know. :smile:
    Last edited: Jan 11, 2010
  15. Jan 11, 2010 #14


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    No. Experiments have demonstrated membrane potential is sustained even when ions pumps are poisonned and ATP is missing.
  16. Jan 11, 2010 #15
    Thanks a lot for the very detailed respone :smile: It certainly cleared a lot up but I think I just couldn't express my questions properly. I still have bit difficulty in understanding these things

    1. When an action potential reaches a muscle? Only one action potential arrives or many? if it is one, wouldn't that mean the contraction of muscle cells happen one after another? So do muscle cells contract simultaneously(many action potentials arriving) or one by one(one action potential?
    2. I understand from your explanation that cells go back to resting potential after an action potential, but don't they send neurotransmitters before that? So if neurotransmitters are still around wouldn't this come back and activate old cells? How does the body know when to stop this neurotransmitter?
    3. When they send inhibitory neurotransmitters, how do they travel, they cease action potentials so how can they send a signal to a distance far away?
    4. Normal cardiac myocyte

    Cardiac pacemaker
    http://wpcontent.answers.com/wikipedia/en/thumb/7/7e/Pacemaker_potential.svg/354px-Pacemaker_potential.svg.png [Broken]

    Doesn't this show that normal cardiac myocytes have resting potential. If they are having resting potential how could they have automacity?

    I really appreciate your help in this topic :smile: and I hope you continue to help. Thanks :smile:
    Last edited by a moderator: May 4, 2017
  17. Jan 11, 2010 #16
    EDIT: I think what you mean to say is that its resting potential is maintained. That is different than just the term membrane potential. The membrane potential is exactly what I described it as: The difference in voltage between the inside and outside of the cell. It also has no bearing on what I said about this being required for the cell to function properly. I will admit I gave a much too simple explanation it should have included ion channels, ion pumps, exchangers, transporters I could have included Goldmans equations on how resting potential is determined etc. etc. etc. We were specifically talking about neurons however and more specifically what membrane potential means on a neuron. A neuron being an excitable cell can have ACTION POTENTIALS this is still a membrane potential and it is maintained by the various control mechanisms I described (mostly ion pumps).

    So yes, membrane potential on various excitable cells is maintained by ion pumps and channels on a diffusal or electrical basis. It depolarizes and hyperpolarizes using these various methods. So I stand by my previous statement. Resting potential is just a specific membrane potential and it will naturally remain stable if the various control mechanims are broken reason being: resting potentials are relatively stable and with the various control methods not working properly depolarization and hyperpolarization won't occur anyways so it won't need to be regulated at all...
    Last edited: Jan 11, 2010
  18. Jan 11, 2010 #17
    1. It would be many action potentials arriving after the CNS sends it's signal to contract a muscle. The way it is set up is like such:
    1 Motor neuron controls a group of muscle fibres it depends on the muscles purpose to find out how many muscle fibres exactly the neuron is attached to. I.e. in the thigh it could be 1000 muscle fibres to a neuron; for eye muscles it would be MUCH lower say like 5.. This is called a motor unit.
    1 Motor unit will be activated all at once if it receives the impulse and has an action potential, this is the all-or-none principal. No motor-end plates can be inhibited in humans so the only thing the neuron can do is excite them, the only way to stop this is to stop sending action potentials through the motor neuron.
    1 contraction of a muscle will require the recruitment of many motor units, depending on the force required. It will start off with small motor units since these have a lower threshold. As more and more force is required larger and larger motor units will be recruited. This is called Size Principle; we are getting more into kinesiology however.

    Just to let you know the smaller units are generally slow twitch muscles and the larger units are generally fast twitch. Olympic atheletes such as weight lifters or sprinters have the ability to recruit nearly all of their units at once. Other atheletes such as long distance runners have the ability to fire some units and allow others to rest and then fire those units and allow the others to rest. (An interesting side note is that at first with weight training your initial gains in strength are not from increased muscle size or strength but from increased recruitment. :wink:)

    I also noted I made a mistake in my previous post, I was only thinking about generating a weak contraction and stopping it. However when more force is needed the frequency of action potentials will increase. The more frequent they are fired the stronger the contraction, due to something known as force summation. The force from the unit is also stronger due to an increased threshold required to fire the unit. Sorry if I've confused you on this point. If you would like you can look it up as regulation method of rate coding.
    2. The neurotransmitters are destroyed by an enzyme or they just end up back in the originating axon terminal. This is exactly for what your question states, that they could stick around and cause unwanted impulses. Sometimes neurotransmitters do get out of the terminal however for various reasons and they will sometimes cause what is called a mini ESPS or mESPS. The voltage difference caused by these neurotransmitters alone is not enough to cross the threshold. Instead many in combination are required, this also prevents misfiring of cells.

    3. It all happens from your CNS the exact same way that the ESPS were sent out to the motor neuron. They are called ISPSs. These are controlled by your CNS and your brain. (I'm not exactly sure how this works though as I posted before... I don't know how your 'thought' or 'will' transforms into your brain sending these signals.)

    4. Yep that shows exactly what I was talking about. The pacemaker, SA Node, has a higher automaticity, so it fires quicker and therfore controls the rest of your cardiac cells. The reason that they don't go ahead and fire on their own normally is because of the rest period I spoke of for the neurons, it is still needed for the cardiac myocytes and the SA node prevents them from firing on their own by firing again and again faster than they can recover and fire one(really simplified but the gist of it). They do however have automaticity, it's just not on the same level as your SA node, or the other nodes for that matter. Here:
    and here:
    You can even watch cardiac myocytes beat in a culture such as in this video:

    These cardiac myocytes were created from embryonic stem cells. You can notice that most of them are firing, groups of them seem to fire together and lone ones seem to be a bit off pace. When this happens in the heart (cardiac myocytes fire out of pace with the SA node) this creates a dysrhythmia and it is a pathological phenomenon (something is wrong with the heart).
    Last edited by a moderator: May 4, 2017
  19. Jan 12, 2010 #18


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    Hmm, I can't agree.
    1/ ions must be free. Are they?
    2/ The rate of ions pumps is known as 107 ions s-1. Ions are free only 10 or less picoseconds (10-12). Ions pumps are fatefully too slow.
    3/ the system contradicts gauss law.
    4/ what's about osmosis?
    5/ etc....
  20. Jan 12, 2010 #19
    Membrane potential is the difference of voltage between the inside and outside of a cell. It can also be called: voltage accross the membrane and transmembrane potential. If you do not think that these cells utilize ion channels and pumps in order to maintain the potential required (whether it is resting potential or being depolarized or hyperpolarized or anything) then post a new thread with whatever it is you are trying to get accross.

    I can hardly even understand what you are saying if you are saying something I said is wrong the say what exactly is wrong and why it is wrong. Right now your just babbling to me and coming off as a troll.
  21. Jan 12, 2010 #20
    i don't understand exactly what you're saying here, either. one interpretation is that poisoning the ion pumps is sufficient to stop the flow of ions across a cell membrane, and that the cell membrane is a sufficient insulator to maintain the previously established membrane potential for some indefinite time.

    another interpretation is that the ion pumps are not the only mechanism to establish a membrane potential.
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