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Gene controls whether fear is a factor

In the Nov. 18 issue of Cell, researchers report the discovery of a gene that controls the ability to react with appropriate fear to impending danger. As a result, mice lacking the gene stathmin become daredevils of a sort, the researchers report. The basic findings may have general implications for the study of anxiety disorders and potential anti-anxiety drugs, according to researchers.

The researchers found that the gene stathmin--normally present in high levels in a part of the brain called the amygdala--controls both innate and learned fear. Mice without the gene show abnormally low levels of anxiety in situations that should instinctively inspire fear. Stathmin-deficient animals also show less reaction to conditions that have previously proven unpleasant, an indication that the mice lack a normal memory for fear.

"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," said lead author of the study by Gleb Shumyatsky of Rutgers University. "We have now found that stathmin plays a critical role in both learned and innate fear. Knockout mice, which lack the gene, show a decreased memory for fear and fail to recognize danger in innately aversive environments."

By contrast, he added, the mice depleted of stathmin perform normally in a test of spatial learning.

Fear reactions represent a spectrum of behaviors that vary from those that are inborn to those instilled through experience, said the researchers. Instinctive fears--such as fear of heights or predators--are often species specific toward actual or potential threats. In contrast, learned fear results from particular uncomfortable or life-threatening events in the past.

Because fear plays an essential role in survival, memory for fear is easily established, very resistant to extinction, and normally lasts a lifetime,
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Contact: Heidi Hardman
hhardman@cell.com
617-397-2879
Cell Press
17-Nov-2005


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