LOS ANGELES, Oct. 15 (UPI) -- Mark Barad, of the University of California at Los Angeles Neuropsychiatric Institute's Tennenbaum Family Center, and colleagues identified this pathway in mice. Their study could help explain how these animals acquire, express and then release themselves from fear.
As reported in the October 15 issue of the Journal of Neuroscience, the molecular pathway involves a type of electrical switch located in brain cells called L-type voltage-gated calcium channels or LVGCCs. They comprise only one of hundreds of electrical signals in the brain.
The UCLA team injected two chemicals into the mice to block LVGCCs. One is called nifedipine and the other, nimodipine. To trigger a fearful response so they could view this pathway in action, researchers used mild electrical shocks to the foot to frighten the mice.
Study results showed inhibiting LVGCC activity had no effect on the animals' abilities to become afraid and express fear, but it effectively prevented the mice from overcoming fear.
This molecular avenue was found in a region of the brain called the amygdala, an almond-shaped area near the front of the temporal cortex that is key in helping the brain regulate certain feelings, such as fear.
"It's the master area in the brain for the learning and expression of fear, so without it ... wild animals become tame and people are unable to evaluate threats in the environment," Barad told United Press International. "So it's a master switch."
The findings suggest it might be possible to single out other cells in the brain, synapses, which serve as bridges between brain cells, or other molecular avenues that specifically address fear to help treat anxiety disorders in people, Barad said.
"I'm very excited about this," he added. "By targeting this molecule and other molecules that depend on it or communicate with it, we can improve psychotherapy."
Acquiring and overcoming fear are types of learning, Barad explained. Fear is essential to responding appropriately to threats in the environment, which usually are temporary. But anxiety disorders are a result of chronic fear, which does not pose an immediate threat to the individual and which cannot be overcome through normal processes. Behavioral therapy can help teach some patients how to unlearn certain fears. Medications also are used to treat anxiety disorders. Barad said this molecular pathway might also play a role in other psychiatric illnesses.
"This is very important clinically because the problem with phobias in clinical disorders is that they're unwanted persistent fears, but you don't want to block new fears," Kevin LaBar, an assistant professor of neuroscience at Duke University Medical Center in Durham, N.C., told UPI. "Clinically, this new discovery may point to one way we might think of how to develop drugs to treat the problem of persistent fears."
(Reported by Katrina Woznicki, UPI Science News, in Washington)