Researchers at Northwestern University have made an exciting development into the understanding of post-traumatic stress disorder (PTSD) and found that certain drugs appear to prevent the disorder from developing.
PTSD is a debilitating mental illness that affects around 8 million Americans. Symptoms include depression, panic attacks, flashbacks and chronic fear and anxiety. After a traumatic event, the brain becomes over-stimulated and ongoing interactions between certain proteins continue even though they should stop. These interactions cause an exaggerated fear response in the individual who has experienced the trauma.
“People with this syndrome feel danger in everything that surrounds them,” said Dr. Jelena Radulovic, associate professor of psychiatry and behavioral sciences at Northwestern and lead researcher of the study. “They are permanently alert and aroused because they expect something bad to happen. They have insomnia; their social and family bonds are severed or strained. They avoid many situations because they are afraid something bad will happen. Even the smallest cues that resemble the traumatic event will trigger a full-blown panic attack.”
Radulovic's group has developed a mouse model for PTSD, in which mice are exposed to a traumatic (but painless) event, and then exposed to a different event which measures their fear response. The mice maintain PTSD-like fear responses for up to a month.
The group not only identified the molecular cause of PTSD, but found that injecting the drugs MPEP and MTEP (developed by Novartis and Merck, respectively) directly into the hippocampus of these mice within 5 hours of a traumatic event prevented the development of exaggerated fear, and fear response returned to normal.
MPEP and MTEP are both drugs that prevent the uptake of glutamate in neurons. Glutamate is a neurotransmitter that is released after a stressful event and excites neurons. In PTSD patients, the neurons remain excited even when the glutamate has dissipated.
Researchers are excited about the potential of this new type of treatment after the response in the mice after drug treatment.
“The mice’s fear responses were completely normal,” Radulovic said. “Their memories of the stressful event didn’t trigger the extreme responses anymore. This means we could have a prevention approach for humans exposed to acute, severe stressful events.”
The study was published in this month's issue of Biological Psychiatry.
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