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Electrotonic and action potentials

Two different types of changes in the membrane potential of a neuron. Created by Sal Khan.

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  • duskpin ultimate style avatar for user Aanal
    When the potential is dropping is due to the opening of the potassium channels, reaching -80mV there would be a stage when the potential would be a stage when the potential would be at -55mV. In this case, does the sodium channels reopen?
    (25 votes)
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  • orange juice squid orange style avatar for user Abraham George
    How would scientists measure a neurons potential with a voltmeter?
    (15 votes)
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    • purple pi purple style avatar for user Sushma
      A microelectrode, constructed by filling a glass tube of extremely small diameter with a conducting fluid such as KCl, is inserted into an axon in such a way that the surface membrane seals itself around the electrode. A reference electrode is placed in the bathing medium. A potentiometer connecting the two electrodes registers the potential. The potential difference maintained across the cell membrane in the absence of stimulation is called the resting potential ( in humans, −70 mV). A potential difference is registered only when the microelectrode is inserted into the axon; no potential is registered if the microelectrode is in the bathing fluid. Recording of the changes in the membrane potential over time gives a trace and changes over time can be seen and interpreted from the tracing.
      (17 votes)
  • piceratops ultimate style avatar for user Jet Simon
    What is the difference between action potential and graded potential?
    (7 votes)
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  • piceratops ultimate style avatar for user Mark Yazhari
    At , when Sal says "let's say that the sodium channel opens at -55mV," WHY exactly would a sodium channel in real life open at a certain mV threshold?
    (3 votes)
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    • leaf blue style avatar for user dysmnemonic
      The channels are what we call "voltage gated". On the protein, there's a part of its structure called the voltage sensing domain. The charges on the amino acid side chains interact with the membrane potential. When the voltage sensing domain reaches a certain voltage, the interaction between the charges and the membrane potential makes the protein change shape, which then opens up the channel.
      (7 votes)
  • piceratops seed style avatar for user Guilherme Pata
    But why doesn't the signal go backward?
    (4 votes)
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    • leaf blue style avatar for user dysmnemonic
      When the channels reach a certain potential, they slam closed. It takes time for the channel to recover so that it can open again. This means that the signal can't go back the way it came, because the channels behind it can't reopen to conduct it the other way.
      (7 votes)
  • mr pants teal style avatar for user Anya Kotova
    How do voltage sensors on voltage-gated channels work? How do they "feel" the voltage? And how do they relay the signal next to the channel domain?
    (2 votes)
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    • leaf blue style avatar for user dysmnemonic
      The voltage sensing part of the protein is an alpha helix that passes through the membrane, with lots of positively charged amino acids. When the's a positive membrane potential, the charges push the voltage sensor closer to the inside of the cell, which holds the channel closed. When the membrane depolarises enough, the voltage sensor moves and this changes the shape of the protein so that the channel is open.
      (4 votes)
  • mr pants teal style avatar for user Qasim Hashmi
    Wait. So how do the dendrites even respond to a signal. and what would be the defintion of a signal if you are dealing with neurons?
    (3 votes)
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    • winston baby style avatar for user Ivana - Science trainee
      Dendrites are just protrusion of neuronal cells. They have vesicles with neurotransmitters) and receptors for certain neurotransmitters (if we speak of the postsynaptic neuron).

      It works on the basic principle: action potential leads to opening up of Na+ ions and even more entering of Na into the cell, increased voltage opens up vesicles which release neurotransmitters.
      Neurotransmitters are in the synaptic cleft. There they immediately bind to postsynaptic receptors and cause a change of voltage (opening of channels on postsynaptic neuron).

      That way signal is propagated between synapses. Also, where is neuromuscular junction - meaning neuron 'binds' to the muscle fibre, impulse directly go to that fibre and cause sliding of actin over myosin (sliding filament theory).

      In the brain, all impulses are collected and processed, coming to cerebrum or cerebellum. The spinal cord is the integration of all neural impulses - sending away efferent impulses and delivering afferent impulses to the brain.


      Signal just a change in voltage of neuron.
      (2 votes)
  • blobby green style avatar for user jamie.camano
    What would it be like if the resting potential for an organism was significantly lower than the typical neuron -70 mV? How would that change the function?
    (3 votes)
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    • winston baby style avatar for user Ivana - Science trainee
      Do you mean greater number like -100mV, alluding to hyperpolarization?

      First of all, the depolarization of the membrane would be much easier.

      But again, hyperporlarization won't be favored, but even harder to reach.


      On the one side, it might be useful and generate greater conducting velocities, while on the other hand, it might be bad for mechanisms that rely on hyperpolarization, like inhibiting signals.
      (2 votes)
  • male robot hal style avatar for user hardikminocha
    in the previous video, sal said that it is difficult for sodium to come back into the mebrane. so ho can Na flood back into the membrane?
    (2 votes)
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    • blobby green style avatar for user Parker
      In the normal state, when the membrane is at the resting potential, it is difficult for sodium ions to reenter through the sodium channels. But when it reaches the action potential, that opens the sodium channels wide, letting sodium ions flood in temporarily. When the potential reaches the second threshold, the sodium channels close again (and the potassium channels open wide, rapidly restoring the resting potential), so sodium is once again blocked from reentering the cell.
      (3 votes)
  • leaf grey style avatar for user Angela Oh
    I don't really understand what the whole point of this action potential or increase and decrease in voltage is. Can someone clarify what the purpose/goal is?
    (3 votes)
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Video transcript

We've already seen that when a neuron is in its resting state there's a voltage difference across the membrane. And so in these diagrams right over here, this right over here is the membrane. This right over here is the inside of the neuron, and this right over here is the outside. That's the outside and of course this is the outside. This is the outside as well. So if you had a voltmeter measuring the potential difference across the membrane, so if you took this voltage minus this voltage right over here, the voltage between this and that, you would get negative-- let's say for the sake of argument, let's say it would measure, it would average about negative 70 millivolts. So this is in millivolts, negative 70. And I'll do it actually for both of these graphs. We're going to use both of these to describe slightly different, or actually quite different, scenarios. And you could have another voltmeter out here in yellow, and that's a little further out, but that's also going to register negative 70 millivolts. Now let's make something interesting happen. Let's say that, for some reason, let's say that the membrane becomes permeable to sodium. So sodium just starts flooding through. It's going to flood through for two reasons. One, it is a positive ion. It's more positive on the outside than the inside, so positive charge will want to flood in. And the other reason why it'll want to flood in is because there's a higher concentration of sodium on the outside than on the inside. So it'll just go down its concentration gradient. And the reason why we have a higher concentration gradient on the sodium on the outside than the inside, we've already seen, is because of the sodium potassium pump. But anyway, so you're going to have this increase. You're going to really have this spike in positive charge flowing. And then what's going to be the dynamic then inside the neuron? Well, if you have all this positive charge right over here the other positive charge in the neuron is going to want to get away from it. And this is not just in the rightward direction. It's really going to be in all directions. In all directions the positive charge, they're going to want to get away from each other. So this one's going to move that way, and then that's going to make that one want to move that way, which is going to make that one want to move that way. So if we let some time pass, what's the voltage going to look like on this blue voltmeter? Well after some time, because more and more positive charges are trying to get away from these other ones right over here as the concentration of these positive charges spread out, you're going to see the voltage start to increase. And then as they fully get spread out then it might return to something of an equilibrium. And then if we go a little bit further down the neuron a little more time will pass before you see a voltage increase, but because this thing is just getting spread out across more and more distance, the effect is going to be more limited. You're not going to see as much of a bump in the voltage over here than you saw over here. And this type of spread of, I guess you could say a signal, is called electrotonic spread. Let me write that down. Or this is the spread of an electrotonic potential. So there's a couple of characteristics here. One, it's passive. This part that we drew right here, this isn't the electrotonic spread. The electrotonic spread is what happens after that. Once you have this high concentration here, the fact that a few moments later you're going to have a higher concentration of positive charge here, and a few moments later a higher positive concentration here. This is a passive phenomenon. So this thing right over here, it is passive. And it also dissipates. The signal gets weaker and weaker the further and further you get out because this stuff just gets further and further spread out. So it's passive and it dissipates. Now let's play out this scenario again, but let's also throw in some voltage-gated ion channels right over here. So let's say this right over here that I'm drawing, let's say this is a voltage-gated sodium channel. Let's say it opens at negative 55 millivolts. So that would be right around there. So that is when it opens at negative 55 millivolts. Let me draw that threshold there. And let's say it closes at positive 40 millivolts, right over there. I'm just trying to show the threshold. And let's say we also have a potassium channel too, right over here. So this is a potassium channel, the infamous leaky potassium channels, which are the true reason why we have this voltage difference across the membrane. But this potassium channel, let's say it opens when this one closes. So it opens, just for the sake of argument, these aren't going to be the exact numbers but to give you the idea, at positive 40 millivolts. And let's say it closes at negative 80 millivolts. So that one opens up here, and then it closes down here. Now what is going to happen? Well just like we saw before-- Let's let our positive charge flood in here at the left side of this neuron, I guess we could say, and then because of electrotonic spread, a little bit later you're going to have the potential across the membrane at this point is going to start to become less negative. The potential difference is going to become less negative, just like we saw right over here. So it's going to become less negative. But it's not just going to be just a little bump and then go back down, because what happens right when the potential hits negative 55 millivolts? Well then it's going to trigger the opening of this sodium channel. So the sodium channel is going to open because the voltage got high enough, and so you're going to have sodium flood in again. So what's that going to do? Well that's going to spike up the voltage. So it's going to look something like that. It's going to keep flowing in, keep flowing in. The voltage is going to get more and more positive. Because remember, this is going to be flowing in for two reasons. One, there's just more charge. It's more positive outside than the inside so it's going to go across a voltage gradient, or go down the voltage gradient, or the electro potential gradient, but also there's a higher concentration of sodium out here than there is in here because of the sodium potassium pump, and so it'll also want to go down its concentration gradient. So it's just going to keep flowing in even past the point at which you have no voltage gradient, but because of the concentration gradient it's going to keep going. But then, as you get to positive 40 millivolts, this channel is going to close. So that's going to stop flooding in. And you also have the potassium channel opening. And the potassium channel, now you're more positive on the inside than the outside, at least locally right over here. And so now you're going to have this positively-charged potassium ions want to get out, want to get out from this positive environment. And so the voltage is going to get more and more negative, and it's going to go beyond neutral because potassium is going to want to go down, not just its voltage gradient, it's going to do that while it's positive on the inside and negative on the outside, or more positive on the inside than it is on the outside, but it'll also want to go down its concentration gradient. There's a higher concentration of potassium on the inside than on the outside because of the sodium potassium pump. So the potassium will just keep going out, and out, and out, and out, and then at negative 80 millivolts the potassium channel closes, and then we can get back to our equilibrium state. Now why is this interesting? Well we had the electrotonic spread up to this point. But the signal would just keep dissipating and keep dissipating, and if you get far enough it would be very hard to notice that signal. And so what this essentially just did is it just boosted the signal again. It just boosted the signal, and now, a few moments later, if you were to measure the potential difference-- because these things are trying to get away from each other again, once again you have electrotonic spread-- if you were to measure the potential difference across the membrane where this yellow voltmeter is, then you're going to have-- So where that yellow one is, before it had just a little dissipated bump here, but now it's going to have quite a nice bump. And if you actually had another voltage-gated channel right over here, then that would boost it again. And so this kind of very active boosting of the voltage, this is called an action potential. You could view this as the boosting of the signal. The signal is spreading, electrotonic spread, then you trigger a channel, a voltage-gated channel, then that boosts the signal again. And as we'll see, the neuron uses a combination, just the way we described it here, in order to spread a signal, in order for it to have the signal spread, in order to obviously to spread passively, but then to boost it so that the signal can cover over long distances.