Saltatory conduction in neurons | Human anatomy and physiology | Health & Medicine | Khan Academy

By Paul Henry / in , , /

Now that we know how a signal
can spread through a neuron, through an electrotonic
potential and action potential and combinations
of the two, let’s put it all together
by looking again at the structure of a neuron,
the anatomy of a neuron, and thinking about why
it has that anatomy and how it all can work. So we’ve already talked
about the dendrites as being where the
neuron can be stimulated from multiple inputs. If we’re in the
brain, these dendrites might be near the terminal
ends of axons of other neurons. If we’re some type
of sensory cell, these dendrites
could be stimulated by some type of sensory input. But let’s just say, for
the sake of argument, they are stimulated in some way. And because they’re
stimulated in some way, it allows positive ions
to flood into the neuron from the outside. As we know, there’s a
potential difference. It’s more negative
inside of the neuron than outside of the neuron. And so if a channel
gets opened up because of some
stimulus, that would allow positive ions to flow in. And the primary positive
ions we’ve been talking about are the sodium ions. Maybe this is some
type of sodium gate that gets opened up
because of this stimulus. So when that happens, you
will have electrotonic spread. You will have an electrotonic
potential being spread. So let’s say that
we had a voltmeter right here on the axon hillock. It’s kind of the hill that leads
to the axon right over here. So what you might see happening
after some amount of time– so let me draw. So let’s say this is our
voltage in millivolts across the membrane–
our voltage difference, I should say. This is the passage of time. Let’s say the stimulus
happens at time 0. But right at time
0, we haven’t really noticed it with our voltmeter. Our voltage right across the
membrane right over there is at that equilibrium,
negative 70 millivolts. But after some small
amount of time, this electrotonic potential
has gotten to this point, because all of these
positive charges are trying to get
away from each other. It’s gotten to that point. And you might see a
bump in the voltage– in the voltage difference,
I guess I should say. This thing might go up. So it might look
something like that. Now, that by itself
might not be– we might have gotten the
voltage difference low enough, I guess we could say. Or we might not have gotten
the voltage inside of the cell positive enough in order to
trigger the voltage-gated ion channels. And so maybe nothing happens. Maybe this right over here,
this is negative 55 millivolts. And so that’s what you have
to get the voltage up to, the voltage difference
up to, in order to trigger the ion
channels right over there. So those are the sodium channels
to get positive charge in. Here’s the potassium channels
to get the positive charge out. The axon hillock
has a ton of these, because these are really there. Once they get triggered,
they can trigger an impulse that can then go
down the entire axon, and maybe stimulate other
things, maybe in the brain or whatever else this neuron
might be connected to. So maybe that stimulus by
itself didn’t trigger it. But let’s say that there’s
another stimulus that happens right at the same
time, or around the same time. And that happens. And on its own, that
might have caused a similar type of
bump right over here. But when you add
the two together and they’re happening
at the same time, their combined bumps
are enough to trigger an action potential
in the hillock, or a series of action
potentials in the hillock. And so then, you really have,
essentially, fired the neuron. So now all sorts
of positive charge gets flushed into the neuron. And then purely through
electrotonic spread, you will have this electrotonic
potential spread down the axon. Now, this is the
interesting part, because we can think
a little bit about, what is the best way for
an axon to be designed? In general, if you’re trying
to transfer a current, the ideal thing to do is, the
thing that you’re transferring the current down should
conduct really well. Or you could say it
has low resistance. But you want it to be
surrounded by an insulator. You want it to be surrounded. So if this was a
cross section, you want it to be surrounded
by an insulator that has high resistance. And the reason is because
you don’t want the potential to leak across your
membrane– high resistance right over here. If you didn’t have something
high resistance around it, your current would
actually go slower. This is true if you’re just
dealing with electronics. If you just had a bunch of
copper wires on one side, and you had some
copper wires that were surrounded by a
really good insulator, a really good resistor– for
example, plastic or rubber of some kind. The current is actually going
to have less energy loss. It’s going to travel
faster when it’s surrounded by an insulator. So you might say, OK, well gee. The best thing to do would be
to surround this entire axon with a good insulator. And for the most
part, that is true. It is surrounded by
a good insulator. That is what the
myelin sheath is. So let’s say we want to surround
this whole thing with just one big grouping of Schwann’s
cells, so one big myelin sheath– which is
a good insulator. It does not conduct
current well. So this right over here is just
one big myelin sheath right over here. Now, what’s the
problem with this? Well, if this axon is
really long– and let’s say, you know, you’re a
dinosaur or something. And you’re trying
to go up your neck, and your neck is 20 feet long. Or even a human being,
we’re a reasonable size. And you’re going several
feet, or even whatever, you want to go a
reasonable distance purely with electrotonic
spread, your signal, remember, it dissipates. Your signal is going to be
really weak right over here. You’re going to have a weak
signal on the other end. It might not be
even strong enough to make anything
interesting happen at these terminals, which
wouldn’t be strong enough to trigger, maybe,
other neurons, or whatever else might need
to happen at this other end. So then you say,
OK, well then why don’t we try to
boost the signal? Well, how would you
boost the signal? You say, OK. I like having this
myelin sheath. But why don’t we put gaps in the
myelin sheath every so often? And then those gaps
would allow the membrane to interface with the outside. And in those areas, we could
put some voltage-gated channels that can release
action potentials, in order to essentially
boost the signal. And that’s is exactly what the
anatomy of a typical neuron is like. So instead of just one big
insulating sheath like this, it would– let me
make some gaps here. Whoops, I’m going
to do that in black. So actually, let me
just draw it like this. Let me just erase this. So clear, and let me clear this. That’s good enough. And so what we could do
is we could put gaps in it right over here where
the axon, the axonal membrane itself can interface
with its surroundings. And of course, we
know we call those gaps the nodes of
Ranvier, or Ran-Veer. I’m not really sure
how to pronounce it. So let me put
those gaps in here. So you put those gaps in here,
so these are the myelin sheath. And this right over here
is a node of Ranvier. These are nodes of
Ran-Veer, or Ranvier. And right in those little nodes,
right in those nodes, right where the myelin
sheath isn’t, we can put these voltage-gated
channels to essentially boost the signal. If the signal had to
go electrotonically all the way over here,
it’d be very weak. It’s going to dissipate
as it goes down, but it could be just strong
enough right at this point in order to trigger these
voltage-gated channels, in order to essentially boost
the signal again, in order to trigger an action
potential, boost the signal. And now the signal
is boosted, it’ll dissipate, dissipate,
dissipate, boost. And it’ll boost right
over here again. And then it’ll dissipate,
dissipate, dissipate, and boost. Dissipate, dissipate, boost. And so by having
this combination, you want the myelin sheath. You want the insulator in
order to keep the transmission of the current to fast, in order
to have minimal energy loss. But you do need these areas
where the myelin sheath isn’t in order to boost the signal, in
order for the action potentials to get triggered, and so your
signal can keep being– well, I guess keep being
amplified, if we wanted to talk in kind of
electrical engineering speak. And this type of conduction,
where the signal just keeps boosting, and if you were
just to superficially observe it, it looks like the
signal is almost jumping. It gets triggered here,
then it gets triggered, here then it gets
triggered here, then it gets triggered here,
then it gets triggered here. This is called
saltatory conduction. It comes from the Latin
word saltare– once again, I don’t know how to pronounce. My Latin isn’t too good. But it comes from the
Latin word saltare, which means to jump
around or to hop around. And that’s because it looks like
the signal is hopping around. But that’s not exactly
what’s happening. The signal is traveling
passively through. It gets triggered here
in the axon hillock. Then it travels passively
through electrotonic spread. And then it gets boosted. And you have the
myelin sheath around it to make sure it goes
as fast as possible, and you get very
little loss of signal. And then it gets boosted
at the nodes of Ranvier, because it triggers these
voltage-gated channels again. That triggers an
action potential. And then your
signal gets boosted, and then it dissipates–
boosted, dissipates, boosted, dissipates, boosted, dissipates. Maybe it could even
get boosted again. And then it can trigger
whatever else it has to trigger.

37 thoughts on “Saltatory conduction in neurons | Human anatomy and physiology | Health & Medicine | Khan Academy

  1. It's just funny how you posted this on New Year's Eve 🙂 I call this "DETERMINATION" !!! Thanks for the explanation. It is awesome!

  2. I might be wrong about this, but you seem to imply that the point in saltatory conduction is simply the boosting of the action potential within the axon. From what I've understood, saltatory conduction happens when the opening of a sodium gate at the axon hillock/node of Ranvier (point A) causes a change in voltage polarity at the next node of Ranvier (point B) due to an inrush of sodium ions from outside the myelin sheath at point A. This leads to a lower ionic density at point B (the sodium is "sucked in" at point A), which in turn opens the sodium gates at point B etc, where the same thing happens all over again from B to C, C to D etc. This signal propagates down all the way to the end of the myelin sheath to the axon terminal. In other words, saltatory conduction happens outside the myelinated axon. You give the example of a signal booster to explain it and granted, there is an element of that. However, as I understand it, a more accurate metaphor would be following:

    Imagine a department store on Black Friday, which is situated in a long building that has hundreds of front doors. The store is so popular that it is besieged by its customers, who want to get in and who are waiting at every front door. The employees are freaked out and want to go home, but the crowd outside will rush in if they open any of the doors. One of the employees decides to risk it and opens door 1, which results in the crowd barging in. However, the crowd at door 2 thins out because everybody's trying to get in through door 1, so the employee at door 2 opens his door and tries to escape. The crowd notices him and rushes through door 2 as well. The employee at door 3 notices the crowd thinning in front of his door and does the same thing, etc. etc. So, saltatory conduction in this metaphor would be the employees noticing the crowd thinning in front of their door and opening it. To continue with the metaphor, the crowds rushing in does result in more people in the building (i.e. boosting the signal), but the actual saltatory element happens outside the building, as crowds rush from one open door to the next.

    To summarize, the actual definition of saltatory conduction is the sequential opening of voltage-gated sodium and potassium channels due to changes in ionic density outside the myelinated axon. This does result in the action potential being boosted within the axon, but that's a result of saltatory conduction, not saltatory conduction in itself.

  3. Just one thing to correct in the video. The signal travels faster because the myelin sheets acts a s a capacitor. In other words, once an action potential is triggered at one node it provokes a rearrragment of the electric charges in the capacitor (myellin). The change in charge distribution is immediately transmitted to the other end as a change of voltage and triggers a new action potential at the downward node.  View it as electrostatic charges on a plastic rod. If we change the charge at one end of the rod the charges readjust almost automatically at the other end without having any electrical current flowing through the rod.  It is as if all charges are welded together.  If the myelin sheet is destroyed, (like in multiple sclerosis)  then the voltage spread electrotonically within the neuron and gradually decrease in amplitude over distance to a point where no action potentials can be triggered at the downward node. This later process is much slower.

  4. I've really appreciated this video, thank you. Just a question: when the electrotonic current generates, shouldn't it go in both directions (forward and backward)? I mean, as said in the previous lecture, electrotonic signal generates when sodium – during action potential – goes inside the cell, repelling other positive charges. But what inibits the charges to go in both directions, "left and right", and so creating a sequence of action potential in both directions?

  5. I have literally heard over 15 teachers explain Saltatory conduction. This video surpases them all by 10 fold!! Wow, high quality. The multiple stimulations creating the multiple polarization bumbs on the cell body, and the comparison to copper wire with an insulator were new and so helpful.

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