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.