Anxiety disorders², which include posttraumatic stress disorder¹, social phobias（社交恐惧症） and obsessive-compulsive disorder, affect 40 million American adults in a given year. Currently available treatments, such as antianxiety drugs, are not always effective and have unwanted side effects. To develop better treatments, a more specific understanding of the brain circuits that produce anxiety is necessary, says Kay Tye, an assistant professor of brain and cognitive³ sciences and member of MIT's Picower Institute for Learning and Memory.

 

"The targets that current antianxiety drugs are acting⁴ on are very nonspecific. We don't actually know what the targets are for modulating⁵ anxiety-related behavior," Tye says.

 

In a step toward uncovering better targets, Tye and her colleagues have discovered a communication pathway between two brain structures -- the amygdala（杏仁核） and the ventral hippocampus -- that appears to control anxiety levels. By turning the volume of this communication up and down in mice, the researchers were able to boost and reduce anxiety levels.

 

Lead authors of the paper, which appears in the Aug. 21 issue of Neuron, are technical assistant Ada Felix-Ortiz and postdoc Anna Beyeler. Other authors are former research assistant Changwoo Seo, summer student Christopher Leppla and research scientist Craig Wildes.

 

 

Both the hippocampus（海马）, which is necessary for memory formation, and the amygdala, which is involved in memory and emotion processing, have previously⁶ been implicated⁷ in anxiety. However, it was unknown how the two interact.

 

To study those interactions, the researchers turned to optogenetics, which allows them to engineer neurons to turn their electrical activity on or off in response to light. For this study, the researchers modified a set of neurons in the basolateral amygdala (BLA); these neurons send long projections⁸ to cells of the ventral hippocampus.

 

The researchers tested the mice's anxiety levels by measuring how much time they were willing to spend in a situation that normally makes them anxious. Mice are naturally anxious in open spaces where they are easy targets for predators⁹, so when placed in such an area, they tend to stay near the edges.

 

When the researchers activated¹⁰ the connection between cells in the amygdala and the hippocampus, the mice spent more time at the edges of an enclosure, suggesting they felt anxious. When the researchers shut off this pathway, the mice became more adventurous¹¹ and willing to explore open spaces. However, when these mice had this pathway turned back on, they scampered¹²（蹦跳，奔跑） back to the security of the edges.

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