Deactivating a specific gene transforms meek mice into daredevils, researchers have found. The team believe the research might one day enable people suffering from fear – in the form of phobias or anxiety disorders, for example – to be clinically treated.

The research found that mice lacking an active gene for the protein stathmin are not only more courageous, but are also slower to learn fear responses to pain-associated stimuli, says geneticist Gleb Shumyatsky, at Rutgers University in New Jersey, US.

In the experiments, the stathmin-lacking mice wandered out into the centre of an open box, in defiance of the normal mouse instinct to hide along the box’s walls to avoid potential predators.

And to test learned fear, the mice were exposed to a loud sound followed by a brief electric shock from the floor below them. A day later, normal mice froze when the sound was played again. Stathmin-lacking mice barely reacted to the sound at all.

Neural responses

In both mice and humans, the amygdala area of the brain serves as the control centre of basic fear impulses. Stathmin is found almost exclusively in this and related brain areas.

The protein is known to destabilise microtubule structures that help maintain the connections between neurons. This allows the neurons to make new connections, allowing the animal to learn and process fear experiences, Shumyatsky says. Without it, the neural responses are stilted.

The lack of the protein does not appear to affect other learning experiences, as both sets of mice were able to memorise the paths out of mazes equally well. “This is a good sign for an eventual clinical application that could let people deal with their fears in an entirely different way,” Shumyatsky says.

In 2002, Shumyatsky and colleagues published a study on a similar gene encoding for a protein called GRP. But this protein seems only to be associated with learned fear, and would therefore only have clinical implications for conditions such as post-traumatic stress disorder.

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