12 min Reading Time

Hi there! Today we’ll take a multi-threaded look at the fascinating process of learning - we’ll start with the basics and answer the question “how do neurons work?”, after which we’ll dive right in the wonderful world of neuroplasticity - what it is and how it functions. Finally, we’ll understand how we can use innovative learning techniques for our own daily needs.

As you can imagine, today’s topic is nothing short of complex but just by understanding it a bit better, understanding ourselves a bit better we can open doors that we never knew existed, tap into superpowers we never knew we had. And last but not least, we’ll understand how learning impacts us (hint: more than you might imagine at first!). So let’s dive right in!

Cellular Anatomy - Microcosmos of Neurons

As with many other processes that involve the human organism we need to start our journey with the smallest “living” unit that is part of the system. In this case, as with others, it is a cell - the neuron , the building block of cognition.

A very rough schematic of a neuron. Even so, it's more than enough to give us a general idea.

The typical aspect of a neuron is displayed above: a cellular body with multiple small processes coming out of it forming a sort of star pattern called dendrites and a single long extension, the axon. (1,2) There are variations on this morphology especially in certain tissues with special functions but for now that is all we need to know. The surface of the axon is sheathed in a substance called myelin that has the distinct property of being insulated electrically. There are however gaps at predetermined spaces on the axon that allow arcs of electricity to jump from one end of the cell to another and from cell to cell (we’ll get to this part later a bit).

The neurons intertwine, attaching themselves, either dendrite to dendrite, axon to body, dendrite to axon or any other combination of the 3 forming synapses. If one neuron is a building block, several of them linked together will become the “building”.  The result is a 3 dimensional web that will end up macroscopically shaped like the brain we know. Well roughly, there are other cells and tissues as well that provide an auxiliary or support function that contribute to the shape of the cortex. These support cells however lack an important ability that the neurons do have - being able to communicate with each other via electrical signals or more properly called - action potentials .

That being said we should stop for a second, take a break and just try to visualize the sheer beauty of the cortical architecture. Here, we’ll give you a hand - an artistic yet anatomically accurate depiction of the brain, brain stem and cerebellum by the very talented Greg Dunn.

“Self Reflected” by Greg Dunn. Do look up more of his incredible work.

Action Potentials

Alright let’s get back to work. These electrical signals mentioned before, are called “action potentials” and they are probably one of the most important concept you should understand out of this whole read. They represent the fundamental process that underlie all brain function, not just learning but everything we do, we say, we feel or we experience either voluntarily or not. (3)

We should imagine action potentials as a “wave” of electricity that passes along the neuron from one end to another after which it passes along to another neuron on and on. They are born and kept alive by the flow of ions (Na+, Ca, Cl, etc.) across the outer layer of the neuron - the plasma membrane. In order to understand how these “waves” work we need to look closer at the surface of neuron itself, using some form of magnification.

If we’d go close enough, let’s say... to the point of being able to see individual proteins, we’d find the surface covered with a large number of tubular structures. These canals or more appropriately named ion channels allow selective passage of ions (in this case Na+) to pass through in exchange for other ions (K+). This exchange is the generator and propagator of action potentials. You can think of it as a sort of water dam, although the mechanism is a biochemical one rather than the potential energy of water driving a water turbine and generator. (3)

By zooming in far enough, we can observe ion channels covering the surface of the neuron.

When we think of storing a piece of information we generally think of a Hard Disk Drive or maybe a CD (anyone still remember floppy disks?) however all the information, all the knowledge that we’ve ever known or will ever know is stored as action potentials. Which means that nothing is stored statically in one place, information is constantly moved from one neuron to another via synapses. When we forget something the cause isn’t an erasion, it’s simply the fact that those specific action potentials faded away. If anything we should start associating our brains more with cloud based computing than SSDs! This simply put, is the fundamental truth about knowledge as far as neuroscientific data suggests.

A piece of information that we understand very well is simply a potent action potential going round and round from one neuron to another inside the “web”. While something we just don’t understand yet or don’t remember that well is a very weak action potential. Let’s just call it the perpetual information motion principle.

Unfortunately, there is still a lot we don’t know at this point. For example one of the biggest questions we still have today would probably be “How do these electrical impulses become complex thoughts and actions?”. Even if our understanding of the whole process lacks some integral steps, we do know enough about these neurological mechanisms that we can influence them and improve them. Therefore, “understanding how we understand” isn’t as far off as it might seem at first.

Well, at this point you might be thinking “well nothing that I didn’t already know from my high school biology class”. And yup, you might just be right, but a little revision is priceless (we’ll see why in part 2). It’ll be well worth the slog through the more…“basic” parts, I promise. Now that we’ve sorted the above out, and we grasped some basic concepts of forms and function let’s keep going on to the more practical parts of our talk. We’ll see you there!

Neuroplasticity - Learning and Evolving

Welcome back! If you’ve just read the previous sections you’re good to go, however if you skipped forward a bit and the words “action potential” or “synapse” don’t sound familiar, we recommend you read up a bit on them. They’ll be important going forward.

Neurons and by extension the majority of our functional brain have a very distinct property that make them stand out from most other structures in our body. They can “rearrange” themselves to some degree. “Rearrange” doesn’t quite do it justice, a more proper term would probably be “adapt” or “to be plastic”. Neuroplasticity is just that, a cellular process that lies at the base of our ability to learn, adapt or change cognitively, emotionally and to be able to acquire new skills.

In any case, in this chapter we’ll be talking about this amazing process, and more specifically the two main sub-types of neuroplasticity - Long Term Potentiation (LTP) and Long Term Depression (LTD).

But we shouldn’t get ahead of ourselves yet, firstly we ought to go back down to the level of the neurons and their ion channels, we need to look at the exact point of connection between two such neurons.

The connection between two neurons (synapse) is mediated by neurotransmitters and receptors.

As you can see from above, if we zoom in enough we can see that connection isn’t a tight fusing between the two cells, there is a small gap between them (called a synapse) and on both sides, on the membranes of the two cells there are structures called receptors. A good analogy for these would be that their akin to switches; they get flipped on by a certain impulse and their effect takes place inside the cell that they are attached to. This impulse is actually a chemical that attaches to the receptor and it’s called a neurotransmitter. (1)

There are various types of neurotransmitters in our body, for different places and different functions. Going in detail would be besides the point of this article but suffice to say that neurotransmitter is a chemical that activates a function in another cell through the interaction with membrane receptors (for those of you that would like to know more, the process is based on the NMDA-AMPA Ca+ mediated secondary messaging system loop). (3)  

Long Term Potentiation (3,4)

Putting the pieces of the puzzle (ion channel, neurotransmitter and receptors) together we can tell the whole story. A strong (high frequency) action potential on the first neuron of the synapse will trigger the local release of the neurotransmitter which in turn will cross the synaptic cleft and attach to the receptors on the second neuron. The activated receptors will induce an effect in the second neuron that will result in:

  1. In the short term (immediately): the appearance of an action potential in neuron #2 and thus the forward propagation of the information;
  2. In the long run (days, weeks): the creation of more receptors that will increase the sensitivity of the second neuron. By sensitivity we mean how easily the second neuron will be depolarized in the future in the same conditions.
  3. In the very long run (months, years): the creation of completely new synapses.

This is called long term potentiation - the sum of the effects that neuron #2 suffers after being in a strong synapse with neuron #1. The end result being a better transmission of information as action potentials via the path that these two neurons constitute.  

Long Term Depression (3,5)

On the opposite side if the bond between the two neurons is relatively weak - the action potential on the first neuron is of a relatively low frequency, neurotransmitters will still be released, they will still bind onto the receptors of neuron #2 but they will have different effects:

  1. In the short term (immediately): the action potential still gets passed along albeit becoming even weaker.
  2. In the long run (days, weeks): not only are new receptors not created but existing ones are disabled and removed by neuron #2 thus weakening the link even more.

This is called long term depression - the sum of the effects that neuron #2 suffers after being in a weak synapse with neuron #1. The end result being a worse transmission of information as action potentials via the path that these two neurons constitute.

Setting LTP and LTD side by side we can conclude that there are two very important principles that derive from them that we need to consider in order to fully master and take advantage of neuroplasticity. These are:  

Specificity & Associativity (3,4)


In order for neuroplasticity to take place, a viable synapse between at least two neurons must exist regardless of the type of bond (LTP or LTD). If there is no functional synapse, there is no change, simple enough.


If a strong LTP type bond exists between neuron #1 and #2 and a third neuron comes along and pushes an action potential at the same frequency and with the same timing as one of the other neurons, it will benefit from the existing LTP and will be strengthened as well. In other words, neuron #3 will “piggy-back” onto the LTP of the first synapse and get strengthened as well  even if, by themselves, neuron #1 or #2 combined with #3 would have created a LTD link.

To sum up, the above two principles are some of the most important aspects when it comes to the process of learning or acquiring a new skill. By understanding how neuroplasticity works (by the way, congrats you just did!) we can improve the way we learn and the quality of the information we store. Which is exactly the topic of part 3. So why not keep going now that we have gone through so much already? See you there!

Mnemoneurology - Taking Advantage of Plasticity

Now that we’ve talked a bit about the underlying form and function, we should use our earned knowledge and piece together some practical aspects. After all, what the practical is as important as the theoretical. Mnemoneurology is a term we use to define learning and memory through the facets of neuroscience. If we were to call back to the principle of perpetual information motion and the principles of specificity & asociativity what could we deduce?

  1. Nothing is static; information is a constant flow of electrical impulses; some are stronger than others.
  2. The strength of an impulse is dictated by the frequency that we “utilise” said action potential.
  3. A weak information block can be strengthened by associating it with a stronger one but only under the right circumstances.

In the initial draft of this article we summarized a few study tips and tricks that tap into what we’ve learned so far. We weren’t happy with the outcome, so we decided to write a whole separate article dedicated to studying.

Check out the link above in order to get the full picture. It goes in a lot more detail and is in general more polished than our initial vision for this section.

Before you go , we'd like to thank you for spending the time in order to better understand this fascinating process. We know it wasn't an easy read and there's still a lot to cover but hopefully you got the general idea. that being said, if you did enjoy our content and would like to see more stuff from us, be sure to click on the juicy button below and help us out!

  1. Anthony L. Mescher et. all, “Junqueira's Basic Histology, 14th Ed.” (McGraw-Hill Education), 153-159
  2. KhanAcademy, “Overview of neuron structure and function”
  3. Dale Purves et. all, “Neuroscience, 5th Ed.” (Sinauer Associates), 46-61; 184-207
  4. Leonard E. White, “Medical Neuroscience” (Coursera)
Update Log
  • 18.03.2018 - Initial Publication.
  • 02.06.2018 - Changed the featured image to a much more suggestive one.

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