Electrotonic and action potentials | Human anatomy and physiology | Health & Medicine | Khan Academy
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Electrotonic and action potentials | Human anatomy and physiology | Health & Medicine | Khan Academy

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.

14 thoughts on “Electrotonic and action potentials | Human anatomy and physiology | Health & Medicine | Khan Academy

  1. I'd like to now why the Na+ channel do not opens at the -55mmV on the eletric level dawn, have some special motivation?


  3. Are these potientials going on parallel or separate? I mean does the electrotonic potential trigger the action potential?
    And one more thing that im not sure of.. These Na+ and K+ channels works by active transport or passive? And the meantime the pumps workin also?

  4. That was very helpful. Thank you. But only one remark. I believe that those K channels are just voltage gated channels and not the "leak" channels as you mentions. Leak channels are constitutively active and contribute to the resting membrane potential but they are not voltage gated. I think so. Maybe I'm wrong….

  5. Awesome description. I was wondering though, this doesn't seem to explains the Uni directional nature of neural transmission .

  6. Our professor said that during the action potential the sodium influx stops because there is no more room for sodium and that all the positive charge is inside but it seems wrong, sodium stops entering because the channels are designed to close at about +35mv and if they don't close the influx would continue to reach as high as +60mv of potential.

  7. I think when the membrane is going back to its resting state from 30-40mV, the K+ channels will open slowly and it will go back inside the ICF. The reason for repolarization will be sodium channels inactivating. -Berne and Levy

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