Neuron action potential mechanism | Nervous system physiology | NCLEX-RN | Khan Academy


In this video, I want to talk
about how action potentials are generated the
trigger zone and how they’re conducted down the axon. So I’ve drawn a soma here in
red and one axon in green. And I’ve blown up the
axon to a very large size just so I had some room to draw. Here’s our graph of
the membrane potential on the y-axis and
time on the x-axis. And now I’ve put a couple of
different kinds of ion channels in the membrane of the axon. The first in this lighter grey
are the leak channels that we talked about when we talked
about the neuron resting potential. These channels are
open all the time. They’re not gated. And I have not drawn any
ligand gated ion channels like the neurotransmitter
receptors that occur on the soma
and the dendrites. But to talk about
the action potential, I need to introduce an entirely
new type of channel that I’ve drawn in dark grey
with this little v. And these are voltage
gated ion channels. The membrane of an
axon as many voltage gated ion channels,
most of which open when the membrane potential
crosses a threshold value. So we’ve talked about the
threshold potential before. And all of these numbers may
vary between different types of neurons, but these would
be fairly common values. So many neurons would have
a resting membrane potential of around negative 60 millivolts
and a threshold potential of around negative
50 millivolts or so that I’ve drawn
with a dashed line. And the importance of
this threshold potential is that it determines
if these voltage gated ion channels will open. So when there is enough
temporal and spatial summation of excitatory grad potentials
to get us toward the threshold, here at the trigger zone, at
the initial segment of the axon, so let me just
draw that, that we have temporal and
spatial summation of excitatory
potentials spreading across the membrane of the
soma into the initial segment of the axon, the trigger zone. This voltage gated ion
channel has a mechanism to sense this voltage change. And when the threshold potential
is crossed, it’s going to open. And these are going
to be sodium channels. Recall that the electrical
and diffusion forces acting on sodium ions are
strongly trying to drive them into the neuron. So when this voltage gated
sodium channel opens, sodium is going to
flow into the neuron through the open channel causing
that part of the membrane to depolarize from all
these positive charges now on the inside. This is going to cause an
explosive chain reaction by triggering the
voltage gated sodium channels in the next
piece of the membrane so that more sodium is going
to flow in further depolarizing the membrane and opening the
next voltage gated sodium channel. These voltage gated
sodium channels open very quickly
triggering each other in a wave that rapidly
spreads down the axon. The trigger zone has
the greatest density of these voltage gated
sodium channels which is why action potentials usually
starts at the trigger zone. So many of these voltage
gated sodium channels will open that the membrane
permeability to sodium is dramatically increased. This is going to cause the
membrane potential, which has already gone from
the resting potential to the threshold potential
from the grated potentials, but now that all this
sodium is flowing in through these open channels,
the membrane potential is going to
dramatically rise trying to head toward the equilibrium
potential of sodium, which is usually somewhere around
positive 50 millivolts. This rapid increase in the
membrane potential values is due to these voltage
gated sodium channels. And this is called the rising
phase of the action potential. And in fact, it becomes more
positive inside the neuron membrane during this
period that it’s the reverse of the
resting potential because normally it’s
more negative inside than outside the
neuron membrane. But now so much
sodium has entered, that it’s more positive inside
the membrane than outside. The action potential usually
peaks though some where around positive 40 millivolts. So it doesn’t make it up to the
sodium equilibrium potential that’s often around
positive 50 millivolts. And the reason for that
is that these voltage gated sodium channels
automatically start to close at the
higher potential values so that sodium stops
flowing into the neuron. And after they close, they’re
in a special state called the inactivated
state and they’re unable to open at any membrane
potential for a brief time. The next thing we see happen
to the action potential, basically just as fast
as the membrane potential went from the resting potential
to the peak of the action potential, it then
rapidly descends back toward the resting potential
and then actually goes farther. It goes more negative than the
resting potential and then it levels off. The reason for this part
of the action potential, which is called
the falling phase, is because potassium
starts to exit the neuron and it does so through a
couple of types of channels. The first are the
leak channels that we talked about when we talked
about the resting membrane potential. Now a little potassium as
exiting through the leak channels at the resting
potential, but even more potassium than normal
starts to exit. Because during these parts
of the action potential, the membrane
potential is positive so that during this part
of the action potential, both the diffusion force
and the electrical force are strongly trying to drive
potassium out of the neuron so that more leaves through
the leak channels that normally does during the
resting potential. The second type of channel
that allows potassium to exit are voltage gated
potassium channels. These also open when the
membrane potential crosses the threshold, but they’re
a little slower to open than the voltage
gated sodium channels. So that at first,
all the voltage gated sodium channels
snap open, allowing sodium to rush in causing the rising
phase of the action potential. And then a little
slower the voltage gated potassium channels
open, allowing potassium to flow out of the neuron
contributing to the falling phase of the action potential. And then the action
potential stops falling because now it’s more
negative inside the neuron again so there’s less driving
force pushing potassium out through the leak channels. And also the voltage
gated potassium channels automatically close at
the lower potential values just like the voltage gated
sodium channels automatically closed. But just like the voltage
gated potassium channels were a little slower to open than the
voltage gated sodium channels, the voltage gated
potassium channels are also a little slower to close so
that it takes a little longer for this exit of
potassium to stop. And that’s why there’s
this little bit of a longer period at the end of
the action potential until we kind of
slowly settle back into the resting
membrane potential. Because as these voltage gated
potassium channels are slowly closing, the membrane
permeability to potassium is returning to
the normal amount you get during the
resting potential through the leak channels. And as that permeability
to potassium returns back to the normal resting
potential level, the membrane potential returns
to the resting potential. This movement of sodium
ions and potassium ions across the membrane causing
the wave form of the action potential starts here
at the trigger zone at the axon initial
segment, but then rapidly spreads in
waves down the axon. First, there’s the wave of
depolarization from opening up the voltage gated
sodium channels. So a wave of depolarization
rapidly spreads down the axon, but following right behind
it, right on its heels, is this wave of
hyper-polarization caused by potassium exciting through
the voltage gated potassium channels and the leak channels. So we have the rising phase of
the action potential, the peak of the action potential, the
falling phase of the action potential, and then this
period of hyper-polarization at the end of the
action potential has a couple of names. It can be called the
after hyper-polarization because it’s the
hyper-polarization that happens after this part
of the action potential. But it’s also called
the refractory period. Let me just write that down. Refractory period right there. And it’s called the
refractory period because during this time,
it’s difficult or impossible to trigger another
action potential in that part of the membrane. The refractory period is
divided into two parts. The first part is called the
absolute refractory period. And it’s absolute because the
voltage gated sodium channels when they first close they’re
in a special state called the inactivated state. And they are unable to open
at any membrane potential for a brief time so
that no matter how much excitatory input
comes into the neuron, you can’t trigger
another action potential during the absolute
refractory period. The second part is called the
relative refractory period. And during this
time, the voltage gated sodium channels have
become functional again. They can respond to
depolarization, however, the membrane potential
is hyper-polarized. It’s not yet back to
the resting potential. Therefore, it would take more
excitatory input than normal to trigger an action potential
during the relative refractory period. One important effect of
the refractory period is that action potentials
travel from the trigger zone to the axon terminals. And they don’t turn
around and head right back the other direction
because the membrane right behind the action
potential is refractory. It can’t be triggered by
itself to send the action potential back the other way.

28 Replies to “Neuron action potential mechanism | Nervous system physiology | NCLEX-RN | Khan Academy”

  1. I thought neurons hyperpolarize to a -90mV at the end of the repolarizing phase? You didn't mention anything about that…

  2. Hi, i have a question… i though the absolut period happen since the excitatory stimulus cross the treshold until the end of the repolaritation state, but according to the video all the periods occurs during the hiperpolaritation state, then i got confused about it..  can someone take this over ?  i will be waiting the answer!

  3. I was taught that the equilibrium potential for Sodium is actual around +60 mV, and the resting potential is usually around -70 mV, and that threshold is about -50 mV.

  4. is the trigger zone of the axon you're talking about at 1:40 the axon hillock? or is the axon hillock just for summation of input and then this process you talk about happens after the axon hillock? thanks, great video 🙂

  5. Great video, thank you. You were the only video to differentiate between Leak channels and voltage-gated potassium channels, and that's just the explanation I was looking for!

  6. what is the range of absolute refractory period? does it extend til the lowest point of hyperpolarisation or it stops at the point AP has fallen til the resting potential?

  7. Well, interesting but it seems that at the end of the action potential the axon is full of Na+. It has to flow out maybe by the Na+/K+ pump not mentioned here?

  8. Wait, but i thought the absolute refractory period starts from depolarization to repolarization before it hyperpolarizes and repolarizes again?

  9. Subtitle error in 0:02 in Portuguese (Brazil). It says "ações potenciais" instead of "potenciais de ação".

  10. Sorry, there are more subtitle errors that I took the liberty of listing:

    3:55, 4:24, 4:28, 4:42, 5:06, 5:11, 5:43, 5:54, 5:56, 7:01, 7:33, 7:36, 7:41, 7:48, 8:09, 8:36, 8:59 and 9:16, "ação potencial" instead of "potencial de ação".
    9:06 "ações potenciais" instead of "potencias de ação".
    1:03, 1:15, 3:08, 4:21, 4:26, 5:08, 5:30, 6:55, 8:28 and 8:48 "membrana potencial" instead of "potencial de membrana".

    Seems like every use of those terms is wrong, should be pretty easy to fix.

  11. Are sodium channels ligand-gated or voltage-gated or both? I think initial action potential is triggered by influx of sodium ions through ligand-gated channels activated by binding of acetylcholine. Thereafter, the action potential is propagated through the entire length of the axon by influx of more sodium through voltage-gated channels.

  12. So a quick question, what happens to the excitatory input when the Na Channels are in the inactivated state and neuronal membrane is in the hyperpolarized state.

  13. Its very unclear where the absolute refractory period is at. Isn’t at the part of the wave that starts going way positive?

Leave a Reply

Your email address will not be published. Required fields are marked *