Action Potential

Home / Neurology / Synapses / Action Potential

Original Author(s): Aarushi Khanna

Last updated: 31st January 2021
Revisions: 8

Neurons communicate with each other via brief electrical signals known as action potentials. They are brief changes in
the voltage across the membrane due to the flow of certain ions into and out of the neuron. In this article, we will
discuss how an action potential (AP) is generated and how conduction of an action potential occurs.

The Resting Membrane Potential

The resting membrane potential of cells varies depending on the cell type. For neurons, it typically sits between -50 and
-75mV. This value depends on the types of ion channels that are open and the concentrations of di erent ions in the
intracellular and extracellular fluids during the resting state. In neurons, K+ and organic anions are typically found at a
higher concentration within the cell than outside, whereas Na+ and Cl- are typically found in higher concentrations
outside the cell.

This di erence in concentrations provides a concentration gradient for ions to flow down when their respective
channels are open. Hence, K+ ions would be moving out of the cells, while Na+ and Cl- ions would be moving into the
cell. At the resting state, the cell is mostly permeable to K+, as such this exerts the greatest influence on the resting
membrane potential out of the three ions. Further information on the resting potential generation can be found here.

These concentration gradients are maintained by the action of the Na+/K+ ATPase via active transport, which in turn
allows the membrane potential to be maintained.

© Synaptidude [CC BY 3.0 (https://creativecommons.org/licenses/by/3.0)], from Wikimedia Commons

Fig 1 – Diagram demonstrating the ions involved in setting the resting membrane potential, as well as the direction of the ion concentration gradients.

Generation of Action Potentials

During the resting state, the membrane potential arises because the membrane is predominantly permeable to K+. An
action potential begins at the axon hillock as a result of depolarisation. During depolarisation vvoltage-gated
oltage-gated sodium
ion channels open due to an electrical stimulus. As the sodium ions rush back into the cell their positive charge, pushes
potential inside the cell from negative to more positive.
If a threshold potential is reached, then an action potential is produced. Action potentials will only occur if a threshold
is reached. Hence, they are described as “all-or-nothing“. Additionally, if the threshold is reached, then the maximum
response will be elicited.

Once the cell has been depolarised the voltage-gated sodium ion channels begin to close. The raised positive charge
inside the cell causes voltage-gated potassium channels to open, K+ ions now move down their electrochemical
gradient out of the cell. As the K+ moves out of the cell, the membrane potential becomes more negative and starts to
approach the resting potential.

Typically, repolarisation overshoots the resting membrane potential, making the membrane potential more negative.
This is known as hyperpolarisation. It is important to note that the Na+/K+ ATPase is not involved in the repolarisation
process following an action potential.

Every action potential is followed by a refractory period. This period can be further divided into:

the absolute refractory period which occurs once the sodium channels close after an AP. Sodium channels then enter
an inactive state during which they cannot be reopened, regardless of the membrane potential.

and

the relative refractory period which occurs when sodium channels slowly come out of the inactivation. During this
period the neuron can be excited with stimuli stronger than one normally needed to initial an AP. Early on in the relative
refractory period, the strength of the stimulus required is very high. Gradually it becomes smaller throughout the relative
refractory period as more sodium channels recover from the inactivation.

© By Original by en:User:Chris 73, updated by en:User:Diberri, converted to SVG by tiZom [GFDL (http://www.gnu.org/copyleft/fdl.html)

Fig 2 – Diagram showing the phases of an action potential in relation to the membrane voltage over time.

Propagation of Action Potentials

Action potentials are propagated along the axons of neurons via local currents. Local currents induce depolarisation of
the adjacent axonal membrane and where this reaches a threshold, further action potentials are generated. The areas of
the membrane that have recently depolarised will not depolarise again due to the refractory period – meaning that the
action potential will only travel in one direction.

These local currents would eventually decrease in charge until a threshold is no longer reached. The distance that this
would take depends on the membrane capacitance and resistance:

Membrane capacitance – the ability to store charge. The lower capacitance results in a greater distance before the
threshold is no longer reached.

Membrane resistance – depends on the number of ion channels open. The lower the number of channels open, the
greater membrane resistance is. A higher membrane resistance results in a greater distance before the threshold is no
longer reached.
 © By John Schmidt (Mars) [GFDL (http://www.gnu.org/copyleft/fdl.html)

Fig 3 – Animation to show how an action potential is propagated along an axon.

Myelinated Axons
In order to allow rapid conduction of electrical signals through a neuron and make them more energy-e icient certain
neuronal axons are covered by a myelin sheath. The myelin sheath surrounds the axon to form an insulating layer.
Further information on the myelin sheath can be found here

Along a myelinated axon, there are periodic gaps where there is no myelin and the axonal membrane is exposed. These
gaps are called Nodes of Ranvier. In contrast to myelinated sections of the axon that lack voltage-gated ion channels,
Nodes of Ranvier harbour a high density of ion channels. For this reason, an action potential can only occur at the
nodes.

The myelin sheath speeds up the conduction by increasing the membrane resistance and reducing the membrane
capacitance. Hence, the action potential is able to propagate along the neuron at a higher speed than would be
possible in unmyelinated neurons. The electrical signals are rapidly conducted from one node to the next, where is
causes depolarisation of the membrane. If depolarisation exceeds the threshold, it initiates another action potential
which is conducted to the next node. In this manner, an action potential is rapidly conducted down a neuron. This is
known as saltatory conduction.

© By Helixitta [CC BY-SA 4.0 (https://creativecommons.org/licenses/by-sa/4.0)], from Wikimedia Commons

Fig 4 – Diagram to show how the myelin sheath results in saltatory conduction of an action potential along an axon.

+
Clinical Relevance - Multiple Sclerosis
Multiple sclerosis (MS) is an acquired, chronic autoimmune disorder a ecting the CNS. It results in demyelination,
gliosis, and neuronal damage. Common presentations of the disease are optic neuritis, transverse myelitis, and
cerebellar symptoms such as ataxia.

© By Mikael Häggström, used with permission. (All used images are in public domain.) [Public domain], via Wikimedia Commons

Fig 5 – Diagram demonstrating the main symptoms that multiple sclerosis may present with.

There are three main patterns of disease:

Relapsing-remitting – Patients face episodes of remission (during which no symptoms are present) and exacerbations
of the disease.

Secondary Progressive – Initially the MS is of a relapsing-remitting pattern. However, at some point, the disease
course changes, and the neurological function gradually worsens.

Primary progressive – After the onset of the disease there is A steady progression and worsening of the disease.

There is no known cure for MS however some therapies have proven useful in terms of managing acute exacerbations,
preventing exacerbations, and slowing down disability. For example, high doses of intravenous corticosteroids can
help to relieve symptoms in acute exacerbations.