As people grow up, they are told to go to school and learn about certain topics in certain classrooms. They study for assessments, in the hope of adequate grades which could propel them into subsequent stages in their lives. However, the process of learning itself is commonly overlooked, but it should not be. Learning is a fundamental and imperative element of our lives that humans could not live without. Memory, on the other hand, is what holds our lives together. It is nearly incomprehensible to imagine a world where we could not remember the ideas, elements, or facts that we have previously learned. Improvement would be impossible. Thus, it is helpful for everyone, especially athletes, to take a step back to understand how memory works, both from a practical and biological perspective. 

Firstly, learning is the acquisition of knowledge about the world by experience, study, or instruction, while memory is the process by which this knowledge is retained and reconstructed. 

Up to the early 1970s, the medical world knew very little about the two major types of memory, even lacking a frame of reference for studying the biological bases of memory. Scientists around the world could not come to a conclusion between the two leading, but conflicting approaches that tried to explain how memory is stored or formed: Lashley’s hypothesis in the 1950s and Adey’s approach in the 1960s. This discrepancy caused scientists to begin to use tractable behavioral systems, which yielded novel information and data on how specific changes in neuronal elements of a behavior cause modifications of that behavior within the memory and learning storage and formation processes. Spanning from 1964 to 1979, a handful of simple model systems were beginning to be used to study implicit memory. Some of these included the eye-blink response of rabbits, the bending reflex of cats, the gill-withdrawal mechanism of Aplysia, the escape reflex of Tritonia, and the smell learning process in Drosophila. Altogether, by starting at these simple forms of learning, the way to gain a better understanding of the molecular mechanisms and deeper biological processes of complex learning and memory was paved.

Derived from thorough analysis, the mechanism of encoding and storing short-term memory was discovered to revolve around the neurotransmitter serotonin. When a sensitizing stimulus is initially processed as sensory information, there is an increase in strength in the synaptic connection between the sensory and motor neurons near the stimulated area, which leads to the activation of modulatory neurons that release serotonin into the synaptic cleft of the sensory neuron. As a result, this serotonin increases the concentration of cyclic adenosine monophosphate, also referred to as cAMP, in the sensory cell, triggering the release of the critical neurotransmitter glutamate. By doing so, the connection between the sensory and motor neuron is temporarily strengthened.

Seeking to discover how short-term memory turns into long-term memory, neuroscientist Pier Giorgio Montarolo mimicked the changes in synaptic strengthening produced by behavioral learning by replacing the stimuli previously used with momentary applications of serotonin to the tail. He discovered that there was a slight, temporary increase in synaptic strength and, if repeated, an increase that can last for more than a week. This simple experiment provided insight into the molecular mechanism in which short-term memory is converted to long-term memory, a process called consolidation. 

Long-term memory is the remembrance of events, experiences, and learned ideas from the more distant past. With so many factors and elements intertwined with long-term memory, several branches of long-term memory were created, all revolving around rehearsing ideas or elements of short-term memories to consolidate them into long-term memories. Explicit memory (declarative), episodic memory, semantic memory, autobiographical memory, and implicit memory are all subtypes of long-term memory. 

Highly regarded in the field of neuroscience, the concept of long-term potentiation, also referred to as LTP, is the process by which repetitive stimulation across the synapse causes a prolonged increase in excitability of the synapse.

When someone wants to learn something, a certain threshold of understanding must be passed. On a molecular level, this is visible through NMDA receptors, to which glutamate binds to. Before this threshold is passed, the receptor is unresponsive. However, the passing of this certain threshold leads to the activation of the NMDA receptors, generating a rush of calcium ions which cause a prolonged increase of excitability of the synapse. This process is fundamental to both long-term memory and learning, and it leads to several molecular changes after calcium rushes into the neuron. The main three effects include an increased quantity of glutamate that goes into the dendritic membrane, an increased sensitization of glutamate receptors, and the synthesis of odd neurotransmitters that flow back across the synapse (which eventually leads to the increase of glutamate for future action potentials). This procedure ties to learning because the breaking of the NMDA threshold signifies the moment of understanding of a topic, which is one of the first steps of learning. Regarding memory, the alteration of glutamate and glutamate receptors leads to long-term memory because changes induced by LTP to the receptors are transferred from generation to generation of neurotransmitters (even when the neurotransmitters are degraded and replaced).

After being encoded by repetitive stimulation, rehearsal, or practice, long term memory is considered ‘stabilized,’ and can be recalled by specific triggers or cues. An example of this recollection is if a person sees a specific door handle which triggers a memory that tells them that the door needs to be pulled rather than pushed, without the need to read a sign which reveals the way the door opens. 

Furthermore, long-term memories undergo cycles of destabilization and restabilization according to the reactivation schedule of their traces. These cycles represent the dynamics of memory and the fact that consolidated memory is not necessarily ‘fixed’. As a result, consolidated memories may be modified or modulated: more specifically, they may be weakened, enhanced, or altered. Consolidated memories may also change to parallel other coexisting memory traces, being combined or altered by coexisting long-term memories. Consequently, this process has significant behavioral and clinical effects. The possibilities for trace strengthening or weakening provide insight for new strategies for learning and memory (to make these processes more efficient and flexible), diseases dealing with abnormally consolidated memories, and memory impairments in general. 

It is believed that long-term memories always have the possibility of being forgotten. Experimentally, it is extremely difficult to differentiate between forgetting and failing to retrieve memories, giving way to several theories and hypotheses. There are two main theories that attempt to explain how long-term memories may be forgotten. The first of which is the decay theory, which details how memories simply decay and deteriorate over time. The second theory, titled the interference theory, suggests that the learning of related items causes interference with subsequent forgetting of one or both items. Although these theories seem promising to some, they have relatively little experimental evidence that grants them support. 

Specific parts of the CNS have specific functions regarding memory development. These structures are connected via neuron signaling, and it is the pattern and strength of these connections that permit the storage and retrieval of encoded information. Functional imaging technologies such as fMRI and PET scans allow researchers to receive an inside view of the structures involved in the process of stimulus encoding that leads to memory. 

The basal ganglia, the cerebellum, and the association cortices are examples of structures that play an essential role in procedural memory as they are intertwined with our motor control and adjustment. Procedural memory is a branch of long-term memory that revolves around certain activities people learn through practice or repetitive exposure to a series of motor outputs.  

On the other hand, working memory, which is temporary memory used to store and manipulate information that may or may not be encoded into one’s long-term memory, revolves around the hippocampus. Mainly responsible for visuospatial processing, the hippocampus has several, possible, saturating mechanisms of working memory. The functions of the hippocampus further divide if you break it up with a longitudinal axis, as the posterior hippocampus is related to visuospatial detail in specific memories, while the anterior hippocampus is correlated with the remembrance of a location or a general concept. The parahippocampal, entorhinal, and perirhinal cortices also work with the hippocampus in operating spatial cognition. 

The final brain structure that will be specifically discussed in this paper is the amygdala, which works with the emotional aspects of memory, like pleasure, fear, or pain. This area of the brain allows animals to differentiate between positive and negative memories as both noxious and rewarding stimuli have displayed increased activity within certain areas of this structure. Noting if a memory was ‘good’ or ‘bad’ is crucial because of its implications on other biological branches. For example, the emotional aspect of memory relates to the fight or flight response, as more negative stimuli will lead to memories being more easily remembered among an organism, while rewarding or positive stimuli may increase retention in humans.

With all the good that comes with learning and memory, the processes seem to fail at times. This is primarily due to the malfunction of components that operate learning and memory. One example of this is how damage to the medial temporal lobe, the hippocampus area specifically, seems to create difficulty with the creation of new memories. With patients’ short-term memory impaired, patients with damage to this area quickly forget memories and often commit mistakes, even after receiving a similar stimulus multiple times. Researchers suggest that this is because the working memory capacity of these patients is being exceeded, given that too much information is provided in a short amount of time. Korsakoff syndrome is another example of when information processing fails. Marked by anterograde amnesia, individuals with this disease cannot retain new information. The amnesia may also be more patchy or variable when not progressively developing. Pathological changes are most significant in the hypothalamus, mammillary bodies, medial thalamus, and periaqueductal gray matter, which all lead to difficulty in information storage. Korsakoff syndrome is caused by chronic thiamine deficiency, and it is often connected with alcoholism. Overall, it is crucial to observe the failures of learning and memory as it will help us understand the central concepts of the processes. 

All in all, the processes of memory and learning are so often overlooked, despite our constant reliance on them to live a normal life. These processes are multiple dimensional and rely on many interactive subprocesses to properly function. It is important to apply the biological aspect that explains learning and memory to our daily lives to make things easier and more simple. From an athletics standpoint, athletes should be informed on such topics so that they may find ways to implement these aspects of memory and learning to enhance their performance and maximize their efficiency. 

Works Cited

Alberini, Cristina M., and Joseph E. LeDoux. “Memory Reconsolidation.” Current Biology, Cell Press, 9 Sept. 2013, www.sciencedirect.com/science/article/pii/S0960982213007719.  

Almaraz-Espinoza, Alejandro. “Physiology, Long Term Memory.” StatPearls [Internet]., U.S. National Library of Medicine, 26 July 2020, www.ncbi.nlm.nih.gov/books/NBK549791./

Crowder, James A., and John N. Carbone. “Long Term Memory.” Long Term Memory - an Overview | ScienceDirect Topics, 2015, www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/long-term-memory. 

Eicher, Tracy J. “Korsakoff's Syndrome.” Korsakoff's Syndrome - an Overview | ScienceDirect Topics, 2009, www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/korsakoffs-syndrome.  

Kandel, Eric R., et al. “The Molecular and Systems Biology of Memory.” Cell, Cell Press, 27 Mar. 2014, www.sciencedirect.com/science/article/pii/S0092867414002906.