By Vithusan Kuganathan

Memory and your ability to learn are often fairly abstract concepts; however, there is a scientific basis to the activity of your brain and the consolidation of memory which contributes to one’s innate ability to learn. This article hopes to explain the science behind learning and break down any jargon encountered.

Long term potentiation (LTP) is essentially a model for learning and memory, which demonstrates a significant link between synaptic innervation and the ability to consolidate information into memory. Much like many neurological processes we possess, the ability for LTP has stemmed from the interaction of different hormones within the brain, most notability 5-HT (Serotonin) and DA (Dopamine). Hebbian plasticity offers a more refined explanation of what exactly is going on. Hebbian plasticity states, “When an axon of cell A is near enough to excite cell B or repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased”. This acted as a foundation for the development of the theory of synaptic plasticity. Synaptic plasticity essentially refers to modifications to synapses (the ends of neurons and the space between them) as a result of repeated innervation and is a theory surrounding the exact nature of learning and how we actually consolidate information.

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But what exactly causes a change in the morphology of the synapse. As with many models, there are varying ideas. One of the generally approved theories is the holo-enzyme (an enzyme with a non-protein component) β-Calmodulin Dependent Kinase Type II. These tend to be expressed around inhibitory neurons. Changes in membrane potential, which are moderated by Ca2+, cause the β-CaMKII to dissociate from a molecule, and it’s this dissociation which is thought to regulate synaptic plasticity. Changes in membrane potential (activation of Ca2+ channels) are caused by synaptic innervation. Therefore, it stands to reason that going over something does in fact contribute to better retention of information, as you’re activating the synapse and changing its shape which leads to you learning whatever it is you’re trying to learn.

Let’s move back to the idea of Hebbian learning. Hebbian learning is so interesting because the brain is such a complex organ. It will never be the case that a single neuron is activated, so many neurons are being operated throughout the brain, each exciting one another, leading to several connections forming at once. This also reinforces the principle that we as mammals have such a capacity to learn due to the simultaneous firing of these neurons consolidating information all at once.

However, I can’t talk about memory without mentioning the hippocampus. The hippocampus is known for its role in the consolidation of short-term to long-term memory. Lesions of the hippocampus contribute to impaired cognitive function, with a discernible impact on the spatial learning of rodents. What’s so interesting about this is that the lesions impact the spatial learning of the rodents. The association of place with learning is often disregarded as being an important facet of learning, yet spatial learning was an evolutionary necessity for human beings. Linking on from this idea, stunted hippocampal cell proliferation/neurogenesis was attributed to impaired cognitive function and subsequently, the development of dendritic spines and the integration of the matured neurons into the existing neuronal circuitry is also vital for learning.

Overall, it’s clear that cognition in general is a highly complex process, and by extension, so is memory and learning. Yet it’s almost awe-inspiring, the complexity of this organ which has allowed the human race to develop into what it is today.