Introduction

Neurons communicate with other neurons electrochemically.

If you want to learn more about the specific mechanisms that allow neurons to communicate, keep reading. However, before diving into the exact mechanisms, it is important to understand the anatomy of the neuron as each of its structures plays a key role in communication. Read What Is a Neuron? A Beginner’s Guide to Brain Function (2025)) to learn more.

In this post, I will only cover the first part of how neurons communicate (electro-). Because the process has 2 steps involved, I have decided to split each step into 2 different posts so as not to miss important information to provide a deeper understanding of the topic.

This post will discuss what action potentials are, how they work, and each phase associated with this step in neuronal communication. They are essential for neurons to communicate effectively, serving as rapid and reliable electrical signals that transmit information over long distances without losing strength. They form the foundation of the electro- portion of neuronal communication, enabling critical processes such as sensory perception, movement, and higher cognitive functions.

To understand, the action potential in neuronal communication, it is important to understand what a potential is. If you have not read Neurons Made Simple: Understanding the Brain’s Building Blocks (2025), I strongly advise you to do so.

What are action potentials?

Now, exactly, what are action potentials (APs)? An action potential is a rapid reversal of the membrane potential. This reversal starts a chain reaction that is an important part of neuronal communication. As mentioned in our post linked in the abstract, the typical neuron has a resting membrane potential of around -70mV which is more negative compared to the outside of the neuron. When the neuron starts to depolarise, that is when we can see the beginning of action potential. Before that, let’s understand some things about an action potential.

APs are initiated, or fired, at the axon hillock, propagated, or conducted, down the axon, and end at the axon terminals.

They have 4 important characteristics. First, APs follow their all-or-none property in that if their threshold is met, they occur with full strength or they don’t occur at all. In contrast, local potentials (potentials that only occur in specific regions of the neuron), do not have a threshold so they occur in proportion to the strength of the stimulus.

Second, APs only occur at full strength and never vary in amplitude. Local potentials, on the other hand, can vary in strength, again depending on the strength of the stimulus. From this, we can say action potentials are non-graded and local potentials are graded.

Third, APs are non-decremental in that over long distances they don’t lose strength whereas local potentials decrease in strength the farther they travel.

Finally, the process of firing an action potential can be divided into 3 phases: Stimulus, Depolarisation, & Restoration.

How do action potentials work?

Phase 1: Stimulus

To initiate an action potential, the neuron requires a jump start, a trigger, to start the sequence. It is triggered by a stimulus (or multiple stimuli) at the input zone where its receptors can receive incoming information.

For now, what is important to know is the stimuli trigger an action potential via the activation of ligand-gated ion channels.

Ligand-gated ion channels are proteins embedded in the membrane of a neuron. These are selective channel proteins that only allow certain materials to pass through, in this case, Na+ ions to flow inside the neuron.

They have receptors located on their structure that initiate their action. They open when ligands bind and close when the ligand is released or when nothing is bound to it. Ligands are any substances that bind to a receptor.

When the ligand (acting as a communication molecule) binds to the receptor, it creates a type of potential that starts depolarising the neuron.

Phase 2: Depolarisation

Depolarisation is the process of the neuron becoming more positive in charge. Value-wise, depolarisation is when the milli-voltage of membrane potential approaches 0. A rapid depolarisation occurs when the membrane potential meets the threshold.

The threshold is the point (usually around -55 to -50 mV) at which the neuron initiates the rapid reversal of membrane potential caused by the local opening of voltage-gated ion channels. Local means the opening of channels only occurs in a specific area at a given point (soma + axon hillock).

Voltage-gated ion channels (VGICs) are proteins embedded in the membrane of a neuron that open or close in response to a change in membrane potential. So, when the stimulus depolarises the potential to threshold, it activates VGICs to fully open allowing more Na+ into the neuron causing the action potential.

Starting in the axon hillock, the depolarisation of this portion triggers depolarisation in the following portion of the axon. The ions that enter the first portion leak into and are close enough to the next area, causing an increase in the membrane potential, opening more VGICs, and leading to a wave of depolarisation down the axon till it reaches the terminals.

It is not conducted continuously, like a current in a wire. It is not one action potential being carried in one motion (because then it would be kinetic), but multiple action potentials, in a chain reaction, being created all the way down the axon. Each portion of the axon creates a new rapid reversal when the threshold is met in that area.

The action potential then peaks at around +40 mV due to the rapid influx of Na+ ions. When it peaks, the influx of Na+ through the VGICs slows down but does not stop entirely. This transition us from depolarisation to restoration of the resting membrane potential.

Phase 3: Restoration

In response to the membrane potential becoming positive, the K+ VGICs open causing the release or efflux of these ions out of the neuron. By releasing K+ ions, the neuron restores itself and gets back to homeostasis.

This part of restoration can be defined as repolarisation as the efflux of potassium ions makes the neuron more polar and negative in charge compared to the outside.

With the neuron back to its resting membrane potential, the sodium channels become completely inactive and no longer permit sodium to enter the neuron.

However, during restoration, the K+ VGICs do not close as quickly as the sodium channels because of differences in channel structure. As a result, the neuron enters a state of hyperpolarisation where it becomes even more negative in charge than its baseline. The hyperpolarised potential is around -80 mV or lower.

Hyperpolarisation is characterised by 2 refractory periods. Refractory periods are intervals of time where a neuron experiences complete inactivation or decreased sensitivity to stimuli. For both periods, time may vary depending on the neuron.

The first period is known as the absolute refractory period and typically lasts between 1-2 ms (milliseconds). This phase is marked by its complete inactivation of sodium channels so that no matter how strong a presented stimulus is, an action potential has zero chance of firing.

After an action potential is initiated, the absolute refractory period ensures that sodium channels in the previously depolarized region are temporarily inactivated, preventing the action potential from travelling backwards. This mechanism guarantees that the AP propagates down the axon to the terminals. This period is typically characteristic of repolarisation.

The second period is known as the relative refractory period typically lasting 3-4 ms. It is marked by a decreased sensitivity to stimuli. This is because some sodium channels begin to reset. This means that a stronger-than-normal stimulus is needed to initiate an action potential. Decreased sensitivity creates a temporary limit on how many APs can occur. This period usually occurs during hyperpolarisation.

As the last of the potassium channels begins to close, potassium efflux comes to an end. The sodium-potassium pump then actively restores the concentration of ions which helps stabilise the resting membrane potential.

After this entire process, the neuron is now ready to respond to another stimulus and initiate another action potential.

Conclusion

In conclusion, action potentials are rapid, self-propagating electrical signals that are vital for neuronal communication. In order to initiate, a stimulus must activate ligand-gated sodium channels allowing an influx of sodium depolarising the membrane potential. Once it’s raised to the threshold, local voltage-gated sodium channels open causing the rapid depolarisation and reversal which then conducts down the axon.

When it peaks, these channels close and voltage-gated potassium channels open releasing these ions into the extracellular fluid starting repolarisation. Hyperpolarisation occurs as these channels stay longer than usual but once they close, the sodium-potassium pumps take control once again to restore the resting membrane potential.

From initiation to restoration, APs help facilitate the transmission of information along the axon with rapid succession, forming the foundation of neuronal activity. If you are still wondering how neurons communicate? The answer is electro- (and in the next post) -chemically.

References

Byrne, J. (2020). Resting Potentials and Action Potentials (Section 1, Chapter 1) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy – The University of Texas Medical School at Houston. Tmc.edu. https://nba.uth.tmc.edu/neuroscience/m/s1/chapter01.html ‌

Watson, N. V., & S Marc Breedlove. (2021). The mind’s machine: foundations of brain and behavior. Sinauer Associates/Oxford University Press.

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