The Effects of Stress on Memory

Written at Walt Whitman High School

By Kyle Crichton, Louis Moon


We reviewed experiments and studies available on stress and memory in an attempt to better understand the relationship between the two and how they affect one another. We mainly focused on how stress affects encoding, retrieval, and neurochemistry. We will present empirical findings of what brain parts are most affected by stress and how that affects encoding, retention, and retrieval. We found that stress negatively affects encoding. We also discovered that stress can increase encoding, inhibits retrieval, decreases the production of cortisol. So for all three topics, stress affects memory in either a negative or positive way.


As students, we are expected to retain information we learned that day and apply it to our assignments or projects at a later time. Across all ages and occupations, individuals are stressed about what they have to do, which impacts their cognitive performance. How efficiently we encode, recall and apply the information we are presented, amidst competing stimuli, is evaluated by experiments previously conducted. The research we reviewed considers the biological and psychological relationship between stress and cognitive performance.

Background of Stress

Stress is an instinctive behavior towards a high pressure situation that is caused by hormonal and neurological reactions throughout the body. Hormones such as cortisol, activate and allow us to progress through stressful situations (Corbett, Weinberg, and Duarte, 2017) with our immune systems paying the price. This decrease in immune system function results in sleep and eating disorders, as well as other dysfunctions in the brain (Swaab, Boa, and Lucassen, 2005). Stress is also linked to the body’s fight or flight response, this is what activate if something is threatening us. our bodies start to release hormones and we experience stress. Today we work to understand the effect of stress on the body, and how to reduce it through research and therapy.

Background for Memory

When the body takes in sensory information via touch, smell, noise, image, or taste, the brain has a system to solidify the sensory information into long term memory or forget it all together; this ensures that non-essential memories are forgotten (Chang, Jo and Lu, 2011). First comes the registration for sensory information, called a stimulus. For example, when someone touches your shoulder, your body will send sensory information to your brain through neurons. Once in the brain the signal is transduced, “the translation of a sensory signal in the sensory system to an electrical signal in the nervous system” (Sandi, C., & Pinelo-Nava, M. T. , 2012).

There are two memory groups that the brain can translate information into: short term and long term memory (Bisaz, Travaglia, and Alberini, 2014). The brain sends the message to the prefrontal cortex to be cycled into short term memory, which only lasts for 15-20 seconds. If the brain decides that the information is memorable or important, the message will travel to the hippocampus to be stored in long term memory (Bisaz, Travaglia, and Alberini, 2014).

Recall is the process of the brain taking memories out of long term storage into working memory. Working memory lasts for the same amount of time as short term memory, except it is frequently used. Memory is adversely affected when either the encoding process (everything from stimulation to long term memory) is damaged, or the recall process (long term memory to working memory) is damaged. There are also chemical factors that affect memory, such as stress.

Effects on Encoding

Encoding new memories during stress can both positively and negatively affect one’s encoding abilities. Stress can lead to stronger encoding, but this is not necessarily positive. Due to the survival advantages of remembering stressful situations, human evolution has caused stressful events to be recorded in more detail into memory (Nesse and Young, 2000). In 2008, Mather and Nesmith conducted an experiment in which participants were briefly shown positively arousing (it generated a happy response), negatively arousing (it generated a fearful response), and neutral pictures on a grid. The participants remembered the negatively arousing images more easily than neutral images (Mather and Nesmith, 2008). Stress can enhance classical conditioning, but only for negative stimuli (Shors, 1992). An example of this is learned helplessness. While in some instances this can be advantageous, the same phenomena is also responsible for issues like PTSD (Shors,1992). Some studies have shown purely positive effects of stress on encoding. A 1974 study by Günther Bäumler showed that stress can increase your spatial explicit memory, which is the act of one consciously remembering your environment (Simpson, 2010). In this study the LGT-3 was used which is a test where participants had to memorize a route on a map in one minute while undergoing a stress stimulant and then recalling it. Encoding has also been shown to increase immediately after calming down from an extended stressful period (Schwabe and Vogel, 2010). This only happens for a short period of time (Vedhara, 2000) and when this period happens there is a decreased level of cortisol in saliva (Schwabe and Vogel, 2010). Other studies have found negative impacts of stress on encoding. When you are learning information, if you are under stress it can inhibit the function of long term potentiation. This strengthens synaptic neurons through activity. Long term potentiation is important in memory formation and encoding information into your long term memory (Bliss and Lømo, 1973). Other studies found that stress does not affect memory. Using the Montreal Imaging Stress Test (MIST) which is a series of mental math problems while having to deal with threat components. (Corbett, Weinberg, and Duarte, 2017). The trio found that between neutral, minimally negative aroused, and highly negatively aroused, there were minimal changes in memory or encoding and no pattern between the results (Corbett, Weinberg, and Duarte, 2017). Examples of what might be included in the MIST is really world memory tasks that people do on a daily basis and the test gives varying time for the person to remember the task.

Effects on Retrieval

Chronic stress inhibits memory retrieval in a variety of ways. By studying WWII soldiers, the researchers found that some soldiers had no recollection of the events that had occurred in the war (Elzinga and Bremner, 2002). In 2002, the information gathered by Torrie was assessed, and it was found that prolonged stress at high quantities can cause explicit disorders which can result in memory loss at the specific times they experience high amounts of stress (Elzinga and Bremner, 2002). After being stressed for a long period of time the process that encodes and retrieves memory won’t work properly(Schwabe and Vogel, 2010). This was tested by having one group undergo a mild stressor and take what is known as a free recall and recognition test 24 hours after learning. This basically means that the participants would learn information and encode it properly. Then, one group would undergo stress while the control group did not (Schwabe and Vogel, 2010).

Effects on Neurochemistry

Stress has a variety of damaging effects on neurochemistry. One of the primary biological responses to stress is the release of cortisol. Cortisol is released in response to high blood pressure and blood sugar. Cortisol regulates blood pressure and controls metabolism. It is released when you’re stressed. All cortisol receptors are in the hippocampus, a major part of the brain associated with memory.

The hippocampus is the part of the brain that is affected the most when under stress due to the amount of receptors in the hippocampus (Scoville and Milner, 1957; Asalgoo, Jahromi, Meftahi, and Sahraei 2015). In the hippocampus, both functional and structural damage is possible (McEwen 1999). One example of structural damage is atrophy (Lupien and Lepage, 2001), which is a degeneration of cells in the hippocampus, which leads to the loss of function in the hippocampus. Another example of structural damage is neurogenesis disorder (Lupien and Lepage, 2001), which is associated with schizophrenia (Simpson, 2010) and major depression (Shen, 2004).

The increase in cortisol causes the reduction of dendrites, which is how neurons connect and communicate (Woolley, 2001) as well as the amount of neurons, which means less connections among neurons resulting in decreased communication in the hippocampus (Sapolsky, Uno, Rebert, Finch, 1990). Cortisol also affects structural changes in the synaptic terminal which disables the hippocampus’ ability to reabsorb neurotransmitters (Sapolsky, Uno, Rebert, Finch, 1990). It decreases neurogenesis and the creation of new neurons in the hippocampus tissue. This ultimately has long term effects on the function of the hippocampus (Gould, 1998).

A type of hormone called glucocorticoids are part of the body's natural adrenal gland that inhibits memory. Both cortisol and glucocorticoids are released when stressed. The highest concentration of glucocorticoids can be found in the hippocampus (Scoville and Milner, 1957). Glucocorticoids typically inhibit the hippocampus, prefrontal cortex, and the amygdala (Buchanan and Tranel, 2001). When glucocorticoids affect these brain parts, they inhibit cellular metabolism, which is a chemical reaction that keeps cells alive. Glucocorticoids can also make cells in the hippocampus increasingly sensitive to amino acids or neurotransmitters (Sapolsky and Pulsinelli, 1985). This can negatively affect the hippocampus because amino acids have been found to contribute to atrophy in the hippocampus (Maras, 2014). Lastly, glucocorticoids can increase glutamate, an excitatory neurotransmitter involved with memory, however an excess amount of it can lead to damage or death in a cell.


After looking at the sections of encoding, retrieval, and neurochemistry we now know that when stress is involved, encoding is affected positively and negatively. For retrieval, stress affects it negatively. In neurochemistry, stress inhibits it in multiple ways. Of the three subtopics studies the least amount of information was available in that field. Something to note is that the effects of memory when talking about retrieval had contradicting viewpoints in many different studies, so the results are unclear. Retrieval is very important and apply to students, veterans, and people across all occupations. To conclude, people need to further their knowledge in for retrieval is affected by stress. If we are able to understand this further it can help us understand the most productive way to memorize information without it getting lost and can help society become more productive as a whole.


Asalgoo, S., Jahromi, J. P., Meftahi, G. H., & Sahraei, H. (n.d.). Posttraumatic stress disorder (PTSD): Mechanisms and possible treatments. Springer Link. Retrieved from

Bisaz, R., Travaglia, A., & Alberini, C. M. (n.d.). The neurobiological bases of memory formation: From physiological conditions to psychopathology. National Center of Biotechnology Information. Retrieved from US National Library of Medicine database.

Buchanan, T. W., & Tranel, D. (n.d.). Stress and emotional memory retrieval: Effects of sex and cortisol response. In National center for biotechnology information. Retrieved from US National Library of Medicine database.

Chang, T., Jo, S.-H., & Lu, W. (n.d.). Short-Term memory to long-term memory transition in a nanoscale memristor. ACS Nano. Retrieved from ACS Publication database.

Corbett, B., Weinberg, L., & Duarte, A. (n.d.). The effect of mild acute stress during memory consolidation on emotional recognition memory. National Center Biotechnology of Information. Retrieved from US National Library of Medicine database.

De Kloet, E. (n.d.). Stress: A neurobiological perspective [Fact sheet]. Retrieved from

Elzinga, B.M., & Bremner, J.D. (2002). Are the neural substrates of memory the final common pathway in posttraumatic stress disorder (PTSD)? National Center of Biotechnology Information. Retrieved from US National Library of Medicine database.

Gould, E. (1998). Proliferation of granule cell precursors in the dentate gyrus of adult monkeys is diminished by stress. Proceedings of the National Academy of Sciences of the United States of America. Retrieved from

Lømo, T., & Bliss, T. (1973). Long‐lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Physiological Society. Retrieved from jphysiol.1973.sp010273

Lupien, S. J., & Lepage, M. (n.d.). Stress, memory, and the hippocampus: Can't live with it, can't live without it. US National Library of Medicine National Institutes of Health . Retrieved from

Maras, K. L. (2014). Eyewitness testimony in autism spectrum disorder: A review. US National Library of Medicine National Institutes of Health. Retrieved from

Mather, M., & Nesmith, K. (n.d.). Arousal-Enhanced location memory for pictures. National Center of Biotechnology Information. Retrieved from US National Library of Medicine database.

McEwen, B. S. (n.d.). Stress and hippocampal plasticity. US National Library of Medicine National Institutes of Health . Abstract retrieved from

Nesse, R. M., & Young, E. A. (n.d.). Evolutionary origins and functions of the stress response. University of Michigan Department of Psychiatry. Retrieved from

Sandi, C., & Pinelo-Nava, M. T. (n.d.). Stress and memory: Behavioral effects and neurobiological mechanisms. National Center of Biotechnology Information. Retrieved from US National Library of Medicine database.

Sapolsky, R. M., & Pulsinelli, W. A. (1985). Glucocorticoids potentiate ischemic injury to neurons: Therapeutic implications. US National Library of Medicine National Institutes of Health. Retrieved from

Sapolsky, R. M., Uno, H., Rebert, C. S., & Finch, C. E. (1990). Hippocampal damage associated with prolonged glucocorticoid exposure in primates. US National Library of Medicine National Institutes of Health. Retrieved from

Schwabe, L., & Vogel, S. (2010). Learning and memory under stress: Implications for the classroom. Nature Partners Journal. Retrieved from

Scoville, W. B., & Milner, B. (n.d.). Loss of recent memory after bilateral hippocampal lesions. Department of Neurosurgery, Hartford Hospital, and the Department of Neurology and Neurosurgery, McGill University, and the Montreal Neurological Institute, Canada. Retrieved from

Shen, W., Wang, Z., Punyanitya, M., Gallagher, D., Albu, J., St-Onge, M. P., . . . Heshka, S. (2004). Total body skeletal muscle and adipose tissue volumes: Estimation from a single abdominal cross-sectional image. US National Library of Medicine National Institutes of Health . Retrieved from

Shors, T. J. (n.d.). Learning during stressful times. Nation Center of Biotechnology Information. Retrieved from US National Library of Medicine database.

Simpson, T. C. (2010). Treatment of periodontal disease for glycaemic control in people with diabetes. US National Library of Medicine National Institutes of Health. Retrieved from

Swaab, D., Bao, A., & Lucassen, P. (n.d.). The stress system in the human brain in depression and neurodegeneration. National Center of Biotechnology Information. Retrieved from US National Library of Medicine database.

Wooley, S. M. (2001). Characteristics of gait in hemiplegia. US National Library of Medicine National Institutes of Health. Retrieved from