Stress Hormones and the Implications for Memory

 

Stress can come in many different forms. In animal research it is often identified as psychosocial stress or physical stress. Psychosocial stress is the stress that comes from one’s relationships with others, as well as the social environment in general. For example, stress arises when a person evaluates a situation as personally relevant and perceives that he/she does not have the resources necessary to cope with the given situation.   Meanwhile, physical stress is the stress that causes direct stress on the body, such as chronic pain, illness, lack of sleep, poor nutrition, noise, pollution, alcohol, drugs, tobacco, sugar, and caffeine.¹

There are many different parts of the human brain responsible for the different functions of the human body. Researchers have learned that there are various environmental, behavioral, and physiological mechanisms that influence the brain. They are trying to understand the functions of the human brain and how they are related to the development of Alzheimer’s disease.

 

Overall, mild acute stress can enhance memory acquisition and consolidation.² However, chronic stress can impair these processes. Decreased supply of glucose to the brain impairs memory, and conditions that impair brain glucose metabolism, such as type II diabetes mellitus and Alzheimer’s disease, also cause cognitive impairment.

 

The researchers evaluated the body of literature looking at the genetic influences of stress hormones in neurological disorders and their implications on memory. Their summary article discusses three organs, the hypothalamus, pituitary gland, and adrenal glands, and how their interactions make-up the hippothalamic-pituitary-adrenal axis (HPA).

The HPA forms a major neuroendocrine system that regulates body processes such as digestion, the immune system, mood and emotions, sexuality, energy storage and expenditure, and the body’s reactions to stress. The HPA axis is thus involved in the neurobiology of various conditions, including anxiety disorder, ADHD, insomnia, major depressive disorder, chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome, alcoholism, and more.

Of particular interest to their article is the relationship between the HPA and stress. When the human body is placed in a situation of acute stress, the HPA is activated. This prompts the secretion of epinephrine from the adrenal medulla in the brain. Epinephrine acts by stimulating the hippocampal stress-modulated memory processes and increasing the glucose supply to meet the demands of these processes. Epinephrine stimulates the release of norepinephrine in various regions of the brain, including the hippocampus, medial prefrontal cortex, and basolateral amygdala. The adrenal glands rapidly release glucocortoids, which travel to the hippocampus via the blood stream. The glucocorticoids bind to the mineralocorticoid receptors and glucocorticoid receptors in the brain, with the hippocampus having the greatest concentration of receptor co-localization in the brain. The release of these hormones continues at various concentrations for several hours following the initial event.

The researchers report that both human and animal studies have demonstrated that acute stress plays a facilitative role in the formation of long lasting and powerful memories. Specifically, norepinephrine and glucocorticoids create a biochemical environment in the hippocampus that is conducive to enhanced hippocampal–dependent learning and memory. However, glucocorticoids do not always facilitate learning and memory like norepinephrine does. The timing of the exposure is critical to determining whether the glucocorticoids will enhance or inhibit memory formation. Animal and human studies both have demonstrated that exposure to glucocorticoids during learning facilitates memory, while exposure after learning has the opposite effect. Also, if glucocorticoid stimulation occurs hours before norepinephrine secretion, it will inhibit the memory facilitating effects of the norepinephrine.

Moderate doses of glucocorticoid typically enhance learning, while large doses impair consolidation and recall. Chronic exposure to glucocorticoids can be detrimental, by producing hippocampal atrophy and cognitive deficits. Chronic exposure to glucocorticoids also can induce metabolic dysfunction and insulin resistance. This insulin resistance can lead to type II diabetes mellitus, which can result in further damage to the hippocampal structure, physiology, and function.

Optimal glucose supply and utilization to the hippocampus is critical for memory formation. Decreased supply of glucose to the brain impairs memory, and conditions that impair brain glucose metabolism, such as type II diabetes mellitus and Alzheimer’s disease, also cause cognitive impairment. Tests of self-control also show similar glucose supply limited performance. The mechanism by which increased glucose metabolism facilitates superior hippocampal memory formation is still unclear. It is likely that glucose supports multiple memory processes.

The researchers suggest that for a very short time after a stressor, norepinephrine enhances glucose metabolism to support the demands of increased stress-related memory processing in the hippocampus. In contrast, the same stressor triggers the release of glucocorticoids that act as an off-switch and inhibit hippocampal glucose utilization after initial memory formation. The reversal of stress-induced glucose metabolism by glucocorticoids may restrict the increase of memory processes to the immediate aftermath of a stressor. This may increase the prominence of stress-related events and lead to enhanced memory specifically for the stressful events. Stressful events can produce powerful and long-lasting memories. A deeper understanding of how stress affects the brain may lead to a better understanding of the possible role of chronic stress on the development of Alzheimer’s disease, as well as if reversal of the stress process through stress management techniques can reduce the detrimental physiological processes of elevated stress levels.

 

1. National Institute of Mental Health. Fact Sheet on Stress. http://www.nimh.nih.gov/health/publications/stress/index.shtml. Accessed September 1, 2016.
2. Osborne DM, Pearson-Leary J, McNay EC. The Neurogenetics of stress hormones in the hippocampus and the implications for memory. Frontiers in Neuroscience. 06 May 2015.