Molecules that eliminate fear factor could lead to new panic disorder drugs
WEDNESDAY, July 30 (HealthDay News -- The brain mechanism that turns off traumatic feelings associated with bad memories has been identified by researchers at the University of California, Irvine, who said their finding may lead to the development of new drugs to treat panic disorders.
When a person suffers a traumatic experience, environmental cues often become associated with the bad experience. Subsequent exposure to the same cues can cause fear or even panic attacks, according to study author Rainer Reinscheid, an associate professor of pharmacology and pharmaceutical sciences.
The UCI team, along with colleagues from the University of Muenster in Germany, found that a protein called neuropeptide S (NPS) eliminates traumatic responses to bad memories by working on a group of neurons inside the amygdala, the brain region where negative memories are stored.
In experiments with mice exposed to situations that caused bad memories, the researchers found that blocking NPS receptors in the amygdala made traumatic responses to bad memories persist longer. But when the mice were treated with compounds that activated the NPS receptors, traumatic responses vanished sooner.
The findings are published in the July 31 issue of Neuron.
"The exciting part of this study is that we have discovered a completely new process that regulates the adverse responses to bad memories," Reinscheid said in a UCI news release. "These findings can help the development of new drugs to treat conditions in which people are haunted by persistent fears, such as post-traumatic stress disorder or other panic disorders."
Previous research has shown that erasing major negative experiences may require "new learning," such as exposure to the place where the bad experience occurred. This is the first study to identify specific neurons and molecules that eliminate fear memories from the brain.
The U.S. National Institute of Mental Health has more about post-traumatic stress disorder.
-- Robert Preidt
SOURCE: University of California, Irvine, news release, July 30, 2008
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