Kay Tye, an assistant professor of brain and cognitive sciences and member of MIT's Picower Institute for Learning and Memory, said that the targets that current antianxiety drugs are acting on are very nonspecific.
Tye said that they don't actually know what the targets are for modulating anxiety-related behaviour.
In a step toward uncovering better targets, Tye and her colleagues have discovered a communication pathway between two brain structures - the amygdala 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.
Both the hippocampus, which is necessary for memory formation, and the amygdala, which is involved in memory and emotion processing, have previously been implicated 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 projections 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 predators, so when placed in such an area, they tend to stay near the edges.
When the researchers activated 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 adventurous and willing to explore open spaces. However, when these mice had this pathway turned back on, they scampered back to the security of the edges.
The study has been published in Neuron.
--ANI (Posted on 22-08-2013)