Neuronal action potentials
Do you know what happens during an action potential in the neuron?
We’ll answer this question in episode 2 of this Chalk Talk series on action potentials.
In the neuron, an action potential is produced by temporarily changing the cell
membrane's permeability to sodium and potassium ions.
The resting potential of approximately -70 millivolts is maintained primarily by the
transport of potassium ions.
Concurrently, the extracellular sodium concentration is high,
whereas the intracellular concentration is low.
An action potential begins by the opening of sodium channels in the membrane.
Sodium ions move through these channels down their concentration gradient into the cell.
As a result, the positive charge in the cell increases, whereas it decreases
in the cell exterior.
The charge difference between the interior and exterior of the cell decreases,
resulting in a shift of the potential towards a more positive value.
So, the membrane potential increases but still remains negative.
Once it reaches approximately -55 millivolts, which is the threshold potential, the
voltage-dependent sodium channels also open.
As a result, more sodium ions flow through these channels into the cell.
Accordingly, the membrane potential increases rapidly, and an action potential forms.
This process is called depolarization.
It’s facilitated by the closure of the potassium channels,
which are usually open to maintain the resting potential.
Potassium ions can no longer exit the cell and, therefore,
increase the positive excess charge in the cell.
Hypothetically, sodium ions can flow through the membrane until there’s a balanced concentration on both sides,
yielding a sodium equilibrium potential of +60 mV.
In fact, during an action potential, the membrane of a neuron is polarized to only
+30 millivolts, because sodium channels gradually close before reaching the
maximum possible potential, reducing the influx of sodium ions.
Independent of the triggering stimulus, the maximum value attained always lies at
around +30 millivolts, as soon as the threshold potential is reached
and an action potential formed.
This is generally referred to as the all-or-none law.
However, exceeding the threshold potential not only triggers depolarization but also
prepares for a rapid reduction in the membrane potential after depolarization.
It’s ensured by the delayed opening of voltage-dependent potassium channels.
Accordingly, potassium ions move down their concentration gradient and
out of the neuron.
The declining sodium influx and increasing potassium efflux again decrease
the membrane potential.
This process is termed repolarization because it restores the original
charge distribution across the membrane.
Also, the outflow of potassium from the cell can, theoretically, occur
until the potassium concentration is identical on both sides of the membrane.
So, the membrane potential decreases toward the potassium equilibrium potential
of -98 millivolts.
Similar to depolarization, this minimum potential isn’t fully reached.
Repolarization of the cell stops at a value of about -90 millivolts.
This phase is called afterhyperpolarization.
Its name is derived from the state where the cell's membrane potential is below the
resting potential of -70 millivolts.
This is due to intracellular calcium ions, which entered the cell during depolarization
and now increase the activity of the potassium channels.
As the calcium ions are removed slowly from the cytosol, potassium channels
remain active for a longer period.
Now, afterhyperpolarization has an important physiological role:
It’s part of the refractory period, which is the time after depolarization
in which the cell can’t be excited or is difficult to excite again.
In the absolute refractory period, all sodium channels are closed and inactivated.
During this initial phase, a new action potential in the cell can’t occur,
regardless of how strong the incoming signal may be.
In the relative refractory period that follows, sodium channels can be
reactivated but more charge transfer is needed to reach the threshold potential.
One of the reasons is the more negative potential due to afterhyperpolarization.
Only a stimulus stronger than the original can trigger a new action potential
in the neuron.
Once the voltage-dependent potassium channels close at the end of the refractory
period, the resting potential is re-established.