Exposure to a Single Traumatic Stressor Can Change the Brain
Traumatic stressors could change the brain’s logic, mood, and memory areas.
Posted January 14, 2022 | Reviewed by Devon Frye
- Individual reactions to traumatic stressors vary dramatically due to myelination changes in key brain areas.
- Symptoms that may appear after exposure to stress are avoidance behaviors, hyper-arousal, excessive fear, irritability, and cognitive symptoms.
- Just one exposure to a traumatic stressor can trigger a cascade of changes in brain areas important for memory, emotions, and thinking.
- Severe stressors decrease communication efficiency in logical centers and increase connections in emotional and memory brain areas.
Individual reactions to traumatic stress vary dramatically—from resilient to vulnerable, or from growth to disorder. Some symptoms that may appear after exposure to a trauma include avoidance behaviors, hyper-arousal, excessive fear, irritability, and cognitive symptoms like difficulty focusing. The post-trauma changes can culminate into anxiety and/or mood disorders. However, not everyone who experiences a trauma develops subsequent mood and anxiety disorders.
Just one exposure to a traumatic stressor can trigger a cascade of long-lasting changes in the brain, behavior, and mood. How this cascade of events unfolds after a stressor and what areas of the brain are affected contribute to whether a sufferer develops mood and/or anxiety disorders.
What Stress Does to the Brain
Some of the biological biomarkers that convert exposure to a one-time stressor into a disorder are being identified. Previous studies, for example, have revealed a surprising role for axonal plasticity in stress. Axons make up the communication freeways in the brain; they connect cells to each other and transmit messages from A to B. Myelin encases axons and speeds up the transmission of messages in the brain. Nerves that are covered with myelin can transmit a signal at speeds as fast as 100 meters per second. A myelinated axon of small diameter can transmit information as rapidly as much larger unmyelinated axons.
The brain glial cells responsible for manufacturing myelin are called oligodendrocytes. These glial cells are related to stress in two ways: 1) stress can promote the proliferation of oligodendrocytes in mood- or anxiety-related brain regions and 2) oligodendrocytes express receptors for the infamous stress chemical glucocorticoids.1
The relationship between stress and myelin production is region-specific; some brain areas may increase or decrease the production of myelin in response to stress, yet other areas remain unchanged. For example, stress decreases myelin density in the prefrontal cortex,2 while it increases myelin density in the amygdala3 and hippocampus.4 These results suggest that severe stressors decrease communication efficiency in logical centers in the brain (PFC) and increase efficiency in emotional and memory brain areas.
Interestingly, inhibiting the production of new myelin by the removal of oligodendrocytes in the PFC increases anxious behaviors and impairs the recall of fear memories in mice. In humans, early life stressors such as neglect and institutionalization alter white matter integrity in the PFC and this pathology is correlated with cognitive deficits. In other words, the more alterations in white matter because of early life stressors, the greater the cognitive impairments.article continues after advertisement
All of these findings point to the sensitivity of oligodendrocytes which manufacture myelin to stress. Critically, alterations in the production of these glia cells may be the missing link between exposure to stressors and the development of anxiety or mood disorders.
New Research on Stress and the Brain
Scientists at the University of California, Berkeley, and UC San Francisco conducted a couple of experiments that added much more details to this story.5 Specifically, the researchers wanted to understand the brain mechanisms that are associated with the variable individual responses to a one-time traumatic stressor.
In the first study, rat models were exposed to a single inescapable stressor (fox odor). Just like in humans, after one week after acute stress exposure, animals displayed a variety of behaviors from minimally affected to highly affected by the stressor. Remarkably, only two weeks after the stressor, there were significant changes in the brain, including an increase in oligodendrocytes and myelin in the hippocampus (important for memory) and amygdala (important for strong emotions like fear).
What’s more, the amount of increase in oligodendrocytes and myelin was correlated with anxious behaviors. In other words, larger increases led to more anxious behaviors such as avoidance of places that are reminiscent of the stressor and exaggerated fear responses. Just like in humans, the animals showed different levels of vulnerabilities after the stressor and were stressed in different ways; some showed more avoidance, and some showed more startle and fear.
The study was unique because it also revealed a pathology that is associated with anxious behaviors: increases in oligodendrocytes and myelin in the hippocampus. In fact, increasing these cells in the hippocampus was sufficient for the animals to show anxious behaviors without ever being exposed to a stressor.
How This Might Apply to Humans
In another study by the same group of scientists,5 similar findings were concluded from human participants. A group of trauma-exposed U.S. veterans underwent magnetic resonance imaging (MRI) to investigate the association between the integrity of myelin in the hippocampus and amygdala and stress-related symptoms. Half the participants were diagnosed with PTSD and the other half were not. The symptoms were collected from the Clinician-Administered PTSD Scale (CAPS).article continues after advertisement
Hippocampal myelin positively correlated with PTSD symptom severity; the more myelin in the hippocampus, the more severe the symptoms. Specific symptoms were also associated with pathology in different regions. More pathology in the hippocampus was associated with place avoidance, sleep disturbances, and concentration problems. Pathology in the amygdala was correlated with emotional distress and exaggerated startle and fear.
These findings could lead to treatment and even prevention of PTSD and anxiety disorders after a trauma. Perhaps one day, drug or therapeutic approaches that manipulate oligodendrocytes and myelin production can be prescribed immediately after exposure to a severe stressor to prevent escalation into disorders such as PTSD.
What’s more, inferences from such studies can lead to better diagnostic methods and therefore optimal treatment programs. For example, the MRI technique used in the study could be used with people exposed to a traumatic stressor to monitor the integrity of myelin specifically in areas such as the hippocampus, amygdala, and PFC. Therapy can match the implicated pathology in the brain. Treatments for patients with more pathology in the amygdala could focus on techniques for emotion regulation. In patients presenting pathology in the hippocampus, therapy could focus on weakening associations between places that trigger anxiety symptoms and improve cognitive and sleep difficulties.
(1) Distribution of corticosteroid receptors in mature oligodendrocytes and oligodendrocyte progenitors of the adult mouse brain. J Histochem Cytochem. 2014;62:211–26.
(2) Liu J, Dietz K, DeLoyht JM, Pedre X, Kelkar D, Kaur J, et al. Impaired adult myelination in the prefrontal cortex of socially isolated mice. Nat Neurosci. 2012;15:1621–3.
(3) Ono M, Kikusui T, Sasaki N, Ichikawa M, Mori Y, Murakami-Murofushi K. Early weaning induces anxiety and precocious myelination in the anterior part of the basolateral amygdala of male Balb/c mice. Neuroscience. 2008;156:1103–10.