This blog has written numerous times about the importance of acute stress for increased mental performance (such as here, here, and here). But once stress becomes long-term and chronic, it becomes a hindrance. But more than that, it can lead to mental illness. Scientists have long known of the link between chronic stress and mental illness, but a new study from the University of California Berkeley lends even more evidence to the theory that chronic stress can predispose an individual to mental illness, specifically anxiety disorders and mood disorders.
Scientists already know that stress-related mental illnesses have identifiable structural differences in the brain. For instance, those with posttraumatic stress disorder (PTSD) have decreased gray matter volume in the brain. Gray matter consists mostly of neurons (or brain cells) which carry and process information. But scientists have still yet to figure out how chronic stresses create these long-lasting changes in the brain.
In the experiment led by Daniela Kaufer, assistant professor of biology at UC Berkeley, the team found that those that are chronically stressed produce more white matter and have reduced volume in gray matter, much like those with PTSD. White matter is comprised of axons with myelin surrounding it, which create a network of fibers that interconnect neurons (gray matter).
The team believes this disruption in the balance between white matter and gray matter disrupts brain function and communication in the brain. Essentially, those with chronic stress have more resources to connect neurons but do not have enough neurons to go around. This delicate balance between gray matter and white matter is important to a healthy and functional brain.
The study focused only on one part of the brain, but it is an important part, the hippocampus. The hippocampus regulates memory and emotions, and plays a large part in understanding many mental disorders.
Stress and Brain Connectivity
The novel information that the study revealed is the connection between stress and what it does to brain connectivity. In those with PTSD, the connection between the higher functioning hippocampus and the primitive amygdala (which is responsible for the fight-or-flight response) is amplified. This strengthened connection may help explain why those with PTSD are always on guard and constantly scanning their surroundings for danger.
But when the connection between the hippocampus and the amygdala is strengthened, it also means that the connection from the hippocampus to the other parts of the brain is made relatively weaker. For instance, because the connection between the amygdala and the hippcampus is so strong, the more advanced prefrontal cortex is not able to reach out to the hippocampus to tell the brain to keep its cool. The prefrontal cortex is the part of the brain responsible for complex cognitive thought, decision making, and moderation of behavior, among other things. But all the hippcampus can hear is the amygdala, the primitive region of the brain that is responsible for protecting us from danger.
Neural Stem Cells in the Hippocampus
Scientists previously thought that neural stem cells only mature into either neurons or a type of glial cells called an astrocyte in the hippocampus. However, what scientists found in adult rats surprised them; when exposed to chronic long-term stress, the neural stem cells actually turned into another type of glial cell called an oligodendrocyte, which produces the myelin that sheaths nerve cells. And if we remember from above, myelin surrounds white matter in the brain. This new finding suggests that the olingodendrocytes play a central role in permanent changes in the brain that can cause mental problems later on in life. And in previous studies, oligodendrocyte dysfunction or alterations have been implicated in the pathology of certain mental disorders such as schizophrenia and bipolar disorder. In addition, the number of neural stem cells not turning into neurons can help explain the deficits in learning and memory in those with chronic stress.