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Molecular changes in the brain in the aftermath of a traumatic event may help explain long-term susceptibility or resilience

Social avoidance is a common symptom of PTSD, and scientists working to better understand why have laboratory evidence that while stress hormone levels consistently increase in the immediate aftermath of a traumatic event, there can be polar opposite consequences in parts of the brain down the line.

In response to a significant stressor and a subsequent surge of stress hormones, some rodent models experience the expected short-term increase in the excitability of neurons in areas of their brain key to memory and to how they see their environment, as part of the natural instinct to fight or flee.

Other genetically identical mice instead experience a decrease in neuron excitability in this key area called the dorsal hippocampus, Dr. Chung Sub Kim, neuroscientist at the Medical College of Georgia at Augusta University, and his colleagues report in the journal Molecular Psychiatry.

Too little neuronal activity in the hippocampus has been linked to PTSD in humans; and detailed brain imaging of people with PTSD indicates structural and functional changes in key brain areas, like the hippocampus. Glucocorticoid receptors for the stress hormone cortisol are highly expressed in the hippocampus and have been shown to be more highly expressed in PTSD patients than controls when they reexperience stressful situations.

“We are trying to answer the question as to why hippocampal activity is decreased in PTSD or depressed patients,” Kim says. “We know it happens, but the mechanism we don’t know.”

One of the things they are finding is that, like humans, some mice just seem more susceptible to a lasting impact from a major and/or chronic stressor and that both their behavior and internal molecular response to stress are distinctive from their more resilient peers.

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