A genetic variation found deep in the emotional brain may explain why traumatic events such as combat, natural disasters, and violent personal assaults trigger posttraumatic stress syndrome (PTSD) in some but not others.

Fairly common, some 3.5 percent of adults in the United States suffer from PTSD to varying degrees, with one in three cases considered "severe." It's a major issue for soldiers returning home from tours of duty: 20 percent of Iraq and Afghanistan veterans have been diagnosed with PTSD, according to the Congressional Research Service. Persistent frightening thoughts and memories of their terrifying experiences, trouble sleeping, feelings of detachment and numbness, characterize suffers of the condition — a form of emotional brain damage. They are easily startled, forever fearful.

About half of suffers in the general population receive treatment, compared to more than 57 percent of members of the military who've been diagnosed with PTSD. In both groups, 40 percent receive "minimally adequate" treatment, according to the U.S. National Institute of Health.

Deep within the brain, in the amygdala, fearful memories consolidate in processes dependent on gene regulation and protein synthesis, which if blocked somehow would prevent the development of the condition in those lacking molecularly what the U.S. military sometimes refers to as "resiliency." While today civilian and military clinicians treat sufferers of PTSD only following the onset of debilitating symptoms, researchers say the genetic discovery may lead to an early intervention — administered on a battlefield or roadway accident scene, for example — that would block the formation of so-called fear memories.

"This early intervention would be especially appropriate for individuals at higher risk for PTSD after trauma, such as those with a history of previous trauma or those carrying genetic polymorphisms that have been associated with PTSD risk," the researchers reported Wednesday in the journal Science Translation Medicine.

To develop an animal model for PTSD, researchers immobilized laboratory mice to a wooden board, measuring fear responses as increased "freezing" and increased heart rate so the fear response would be present even without the stimulus. Researchers said the technique caused long-range stress symptoms in the mice analogous to PTSD symptoms in humans, such as long-term impaired declarative memory and enhanced anxiety.

Raul Andero Gali and colleagues from eight institutions across the U.S., then looked at gene expression changes in the mice, finding the OPRL1 gene in the amygdala expresses a molecule called nociceptin. A drug targeting that receptor blocked the development of fear memories in mice.

Moreover, researchers found in the study that non-military people exposed to traumatic events, such as childhood abuse, carried the altered form of the gene, and experienced a core symptom of PTSD — the inability to discern safe environments from dangerous ones. In brain imaging, such sufferers also experienced more activation in areas related to fear and pain.

However, the researchers cautioned that the study doesn't mean the gene is solely responsible for fear consolidation within the brain, but is key to the process. "Our data suggest that early intervention — shortly after fear learning — with a selective, centrally acting [drug] reduces fear memory consolidation," the researchers wrote. "In humans, this may translate to the ability to prevent the likelihood of developing PTSD in the aftermath of trauma."

A drug similar in molecular structure to morphine, but without the undesired and addictive properties of opioids, may prove effective in people, they concluded.

Andero, Raul, Brothers, Shaun P., Jovanovic, Tanja, Chen, Yen T., Salah-Uddin, Hasib, Cameron, Michael, et al. "Amygdala-Dependent Fear Is Regulated By Oprl1 In Mice And Humans With PTSD." Science Translation Medicine. 2013.