Washington, Feb 9 (ANI): Our body's response to stress begins in the brain, and a family of proteins plays a prominent role in regulating this mechanism, suggests a new study.
Alon Chen of the Institute's Neurobiology Department found that one protein in the family - CRF - is known to initiate a chain of events that occurs when we cope with pressure, and scientists have hypothesized that other members of the family are involved in shutting down that chain.
Chen and his team have found, for the first time, sound evidence that three family members known as urocortin 1, 2 and 3 - are responsible for turning off the stress response.
The team created genetically engineered mice that don't produce the three urocortin proteins. Before they were exposed to stress, these mice acted just like the control mice, showing no unusual anxiety. When the scientists stressed the mice, both groups reacted in the same way, showing clear signs of distress.
Differences between the groups only appeared when they were checked 24 hours after the stressful episode: While the control 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 the scientists had observed immediately following their exposure to the stress.
To identify the mechanism for the proteins' activity, Chen and his team tested both groups of mice for expression levels of a number of genes known to be involved in the stress response.
They found that gene expression levels remained constant during and after stress in the engineered mice, whereas patterns of gene expression in the control mice had changed quite a bit 24 hours after the fact.
In other words, without the urocortin system, the "return to normal" program couldn't be activated.
"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," he said.
The findings appeared in the Proceedings of the National Academy of Sciences. (ANI)