Some people just don't seem to make a connection between danger and fear.
You know the type: They climb sheer cliffs and jump out of airplanes that are working just fine.
All well and good if you like that sort of thing. But there's a flip side that's truly problematic. Some people are so afraid of even the slightest danger that anxiety overwhelms them.
With the discovery of a fear factor gene, announced Thursday, scientists have moved a step closer to being able to moderate extreme reactions to fear, and also soothe trauma victims.
The researchers identified a gene in mice that controls reactions to impending danger by firing certain neurons in the brain. Mice that don't have the gene, called stathmin, simply don't react to situations that should scare the rodent pants off them.
Human brains are known to work similarly in the age-old fight-or-flight response to things that raise neck hairs.
"For those who experience fear too much, stathmin-based drugs may provide an important relief," Rutgers University scientist Gleb Shumyatsky told LiveScience. "Also, after trauma these drugs may help to forget bad experiences."
More research is needed, of course. And Shumyatsky points out that very little is known about the intricacies of fright in the human mind.
"While one of the best understood memory-related neural circuitries within the mammalian brain is that which controls fear conditioning, little is known about the molecular mechanisms underlying fear reactions," he said.
The study is detailed in the Nov. 18 issue of the journal Cell.
Key to survival
Fear plays a key role in survival, so all mammals have an efficient memory system to deal with it.
While you can't recall the name of someone you just met, a memory of fright can last a lifetime.
The stathmin gene is normally prevalent in the brain's amygdala. It controls fear of predators, heights and others that are considered instinctive, as well as fears that are learned through specific events.
In the study, mice heard a tone and were given an electric shock. The mice without the stathmin gene reacted less strongly. In a second test, the stathmin-free mice were more likely to venture into open spaces that the others naturally avoided.
As a check, the mice were tested in a maze to make sure those without stathmin hadn't lost the ability to learn and remember in an overall sense. Both groups performed the same.
"The findings provide genetic evidence that amygdala-enriched stathmin is required for the expression of innate fear and the formation of memory for learned fear," Shumyatsky said.
If drugs can be developed to safely mute or enhance the effect of stathmin in humans, it could be used to fine-tune our response to fear, Shumyatsky said.
And what about skydivers?
"I think they are okay and should not take any of these [drugs]," Shumyatsky said. "However, it is possible to think that some will benefit to calm themselves down," he said, perhaps "before critical interviews."
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