What if there were a medication that could simply switch off bad memories?
University of California, Irvine (UCI) researchers have identified the brain mechanism that turns off traumatic feelings associated with bad memories. This finding could lead to the development of drugs to treat Post Traumatic Stress Disorder (PTSD), Panic Disorder, and other Anxiety Disorders.
Rainer Reinscheid, pharmacology and pharmaceutical sciences associate professor at UCI, said,
The exciting part of this study is that we have discovered a completely new process that regulates the adverse responses to bad memories.
These findings can help the development of new drugs to treat conditions in which people are haunted by persistent fears, such as posttraumatic stress disorder or other panic disorders.
What did the researchers find?
Neuropeptide S erases bad memories
Scientists from UCI and the University of Muenster in Germany found that a small brain protein called neuropeptide S is involved in erasing traumatic responses to adverse memories. It works on a tiny group of neurons inside the brain’s amygdala where those memories are stored.
How was the research conducted?
Situations that caused adverse memories
In tests, scientists exposed mice to situations that caused adverse memories. The researchers saw that when neuropeptide S receptors in amygdala neurons are blocked, the traumatic responses to bad memories persisted longer. In turn, when they treated the mice with compounds activating these receptors, traumatic responses disappeared faster.
How we learn to be afraid
Fearful emotions triggered
After a traumatic experience, environmental cues often become associated with the bad experience. Re-exposure to the same environment can trigger fearful emotions or even panic attacks, according to Reinscheid.
Other research has shown that forgetting such negative experiences may require “new learning.” This new learning involves re-exposure to the place where the original experience occurred, but this time without any harmful consequences. This is the basis of treatment with Cognitive-Behavioral Therapy and exposure therapy.
Reinscheid said this process, called the extinction of memories, occurs in both humans and laboratory animals such as mice. Until this study, scientists did not know about the specific neurons and molecules involved with extinction learning of fear memories in the brain.
More information the extinction of fear in the brain can be found in the post, “Important Research Finds Brain Cells Related to Fear.”
Previous work by Reinscheid’s group has shown that neuropeptide S is involved in regulating wakefulness and anxiety. Last year, they found evidence that a particular genetic variant of the neuropeptide S receptor may increase vulnerability to Panic Disorder. The current study appeared in the July 31 issue of Neuron.
What do you think?
A new drug for fears?
For many years, research in Anxiety Disorders took a back seat to studies of depression, schizophrenia and other mental disorders. Finally, there is a great deal of research about Anxiety Disorders going on. Exciting new discoveries are being announced practically every other week. What’s most exciting to me is that these findings may lead directly to a medication that will take away the fear that plagues victims of Post Traumatic Stress Disorder, Panic Disorder and other Anxiety Disorders.
- What do you think about the medication possibilities of this research?
- Was this post too technical? I tried to tone it down as much as I could.
As always, your comments are welcome!
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Resources used in this post:
Medical News Today. (2008, July 31). Minimizing Traumatic Response to Bad Memories. Retrieved August 29, 2008 from Medical News Today Web site: http://www.medicalnewstoday.com/articles/116770.php
Science Daily. (2008, August 2). Traumatic Response to Bad Memories Can Be Minimized. Retrieved August 29, 2008 from Science Daily Web site: http://www.sciencedaily.com/releases/2008/07/080730140625.htm
Vasich, Tom. (2008, July 30). Traumatic response to bad memories can be minimized. Retrieved August 29, 2008 from the University of California, Irvine via EurekAlert! Web site: http://www.eurekalert.org/pub_releases/2008-07/uoc–trt072808.php
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