Study Finds Brain May Have Switch That Regulates Trauma Experiences

Post-traumatic stress disorder (PTSD) is characterized by anxiety, depression, sleep problems and flashbacks. It occurs when an individual experiences or is a witness to a tragic event, which may include anything from being in a car accident or witnessing an assault.

PTSD is often exhibited in soldiers who return from a deployment. However, two individuals can experience the same trauma and go on to have very different experiences. They may have varying levels of PTSD, experience very different symptoms of the disorder, or one may be diagnosed with PTSD and the other not experience any lingering problems related to the event.

Given this varying experience by those who witness or are a victim of a tragic event, researchers in United Kingdom sought to understand what brain functions might be involved in the development of PTSD. It seems that some individuals are protected from the disorder, while others suffer severe symptoms.

Researchers from the University of Exeter Medical School found that a neural mechanism exists that keeps the trauma experienced from developing into PTSD.

Based on the understanding that the brain has a certain level of "plasticity," an ability to regulate itself and adapt to its environment and experiences, the researchers studied stress in mice. They found that stress can cause the brains in mice to reprogram specific receptors found in the amygdale, where emotions are regulated. The same receptors go on to react to the next traumatic event with those changes in place.

The receptors are called protease-activated receptor 1, or PAR1. They act as a command center, giving instructions to neutrons to tell them to stop activity or accelerate activity.

The role of the PAR1 receptor is to instruct the neurons to remain active and provide emotions, when it is in its normal function. When a trauma occurs, however, the same receptors tell the neurons to stop activity and cease emotion production. This braking mechanism is a protection that prevents an organism from experiencing uncontrollable fear.

The function aids in keeping fear under a reasonable control, and not reacting in exaggerated ways to mild threats. For instance, the function keeps a person who had a mildly frightening experience with a dog as a child from experiencing panic whenever they see a dog.

The researchers de-activated PAR1 receptors in a group of mice, who then experienced severe fear reactions to even mild stimuli.

Lead author Robert Pawlak, M.D., Ph.D., explains that the understanding that the receptor can turn on and off the neutrons depending on trauma experiences adds a new level of understanding to how the brain connects fear and emotions.

The findings will be used to develop new research studies to understand how the receptors affect the development of anxiety and depression in humans.

The study’s findings are published in a recent issue of the journal Molecular Psychiatry.