Stress: Why is It A Nuisance For Some But Devastating For Others

Rayshell Clapper for redOrbit.com – Your Universe Online

We live in a world that is constantly on the move. We have things stimulating us all of the time, often leading to overstimulation. We work more and more, and because of technology, often bring that work everywhere, and I do mean everywhere, with us. It is no wonder many people experience stress and stress-related disorders.

As the National Institute of Mental Health defines, “Stress can be defined as the brain’s response to any demand. Many things can trigger this response, including change. Changes can be positive or negative, as well as real or perceived.” And the truth is that more than just change triggers the stress response. Moreover, the stress response can lead to even more dangerous illnesses and disorders like anxiety and depression.

But there is a glimmer of hope in understanding why stress can be so devastating to some, according to Rockefeller University researchers. In fact, the research team found that perhaps there is a molecular mechanism of the so-called stress gap in mice with very similar genetic backgrounds that could lead to a much clearer understanding of certain psychiatric disorders caused by stress, including anxiety and depression. In fact, the research points to new markers that will hopefully better aid in the diagnosis and treatment of stress-related disorders and illnesses.

As the Rockefeller University researchers explain, “In experiments, researchers stressed the mice by exposing them to daily, unpredictable bouts of cage tilting, altered dark-light cycles, confinement in tight spaces and other conditions mice dislike with the goal of reproducing the sort of stressful experiences thought to be a primary cause of depression in humans. Afterward, in tests to see if the mice displayed the rodent equivalent of anxiety and depression symptoms, they found about 40 percent showed high levels of behaviors that included a preference for a dark compartment over a brightly lit one, or a loss of interest in sugar water. The remaining 60 percent recovered well from the stress. This distinction between the susceptible mice and the resilient ones was so fundamental that it emerged even before the mice were subjected to stress; some unstressed mice showed an anxiety-like preference for a dark compartment over a lighted one.”

Specifically, what the study team found was that the mice that were much more highly susceptible to stress had less mGlu2, an important molecule of the hippocampus, which is a region of the brain involved with stress. External experiences affected the expression of the mGlu2 gene, which affected the ability of affected mice to deal with stress and thus the mice exhibited the mouse equivalent of anxiety and depression. This reduction of mGlu2 molecule is important as this molecule regulates glutamate, a neurotransmitter that plays a critical role in communicating messages from and between neurons. Too much glutamate can cause very harmful structure changes to the brain. The research shows that perhaps how the mice reacted to stress is one such harmful change.

The senior author, Bruce McEwen, Alfred E. Mirsky Professor and head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, explained that people and animals have life experiences which can alter the expression of genes. This research more closely confirms that the altered expression of the mGlu2 gene affected how the mice reacted to stress.

Since there are many stress-related disorders and many possibilities of disorders within those, this study is hopeful. In fact, the truth that so many people suffer from stress – be that through a psychological disorder like depression or anxiety or through simple daily struggles like being unfocused or fearful – shows that this study provides a glimmer of hope for diagnosis and treatment. It may even provide what scientists and doctors need to better help predict stress and stress-related disorders. And that is hopeful.

Findings of this research were published September 2 in Molecular Psychiatry.