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Study offers glimpse of how to turn off stress in people exhibiting persistent stress symptoms

Many studies associate the development of stress-related disorders -- like post-traumatic stress syndrome, anxiety disorders, anorexia and depression-- with a stress-response mechanism going haywire.

Soldiers who suffered in combat or ordinary people who experienced stressful or traumatic life events can develop post-traumatic stress syndrome. And although feelings of anxieties are considered normal, and sometimes essential, the problem occurs when there is difficulty recovering from a stress reaction or there is no return-to-normal of certain body functioning, such as slowing of the heartbeat and relaxation of tension.

A recent research that appeared in the Proceedings of the National Academy of Sciences delved into the interaction between the brain and certain body chemicals as influencing stress response. The authors looked into a family of proteins that play a key role in regulating the stress-response mechanism. A protein called CRF is known to set off a chain of events that trigger responses from the brain to the different body systems. The research team has now, for the first time, provided sound evidence that the three CRF family members known as urocortin 1, 2 and 3 -- are responsible for shutting down that chain.

The scientists created genetically engineered mice that did not have the three urocortin proteins. They found that these mice acted just like the normal mice before they were exposed to stress, showing no unusual anxiety. When the scientists applied stress, both the mutant mice and normal mice reacted in the same way, showing clear signs of distress. Differences between the groups were only found 24 hours after the stressful episode: While the urocortin-producing mice had returned to their normal behavior, appearing to have recovered completely from the shock, the engineered mice were still showing the same levels of anxiety observed immediately following stress exposure.

Clearly, the findings suggested that the urocortin proteins had something to do with the return-to-normal behavior, but how, exactly, the proteins do it? To identify the mechanism for the proteins' activity, the team tested both groups of mice for expression levels of certain genes known to modulate fear- and anxiety-linked behaviors. They found that the levels remained constant during and after stress in the urocortin-lacking mice. This is contrary to the gene expression in the urocortin-producing mice which have already changed 24 hours after stress.

The results suggested that deleting all three urocortin genes compromise the stress-response gene regulation circuits so that return-to-normal state cannot be activated. These findings position the urocortins as essential factors in the stress-recovery process.

Study author Dr. Alon Chen remarked, "Our findings imply that the urocortin system plays a central role in regulating stress responses, and this may have implications for such diseases as anxiety disorders, depression and anorexia. The genetically engineered mice we created could be effective research models for these diseases."


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