Mental & Emotional Health
This Is Your Brain on Anxiety
According to the National Institute of Mental Health, over 18 percent of American adults suffer from anxiety disorders. These people suffer from excessive worry or tension that often leads to physical symptoms. A release from the California Institute of Technology reports that previous studies of anxiety in the brain have focused on the amygdala, an area known to play a role in fear. However, Caltech researchers had a hunch that understanding a different brain area, the lateral septum, could provide more clues into how the brain processes anxiety. Their instincts paid off. The team has found a neural circuit that connects the lateral septum with other brain structures in a manner that directly influences anxiety. The findings are published in the January 30th 2014 issue of the journal Cell.
The release quotes corresponding author David Anderson as saying, "Our study has identified a new neural circuit that plays a causal role in promoting anxiety states. Part of the reason we lack more effective and specific drugs for anxiety is that we don't know enough about how the brain processes anxiety. This study opens up a new line of investigation into the brain circuitry that controls anxiety."
Led by Todd Anthony, a senior research fellow at Caltech, the researchers decided to investigate the so-called septohippocampal axis because previous studies had implicated this circuit in anxiety and had also shown that neurons in the lateral septum, a structure located within this axis, “lit up” or were activated when anxious behavior was induced by stress in mouse models. But does the fact that the lateral septum is active in response to stressors mean that this structure promotes anxiety, or does it mean that this structure acts to limit anxiety responses following stress? The prevailing view in the field was that the nerve pathways that connect the lateral septum with different brain regions function as a brake on anxiety to dampen a response to stressors. But the team's experiments showed that the exact opposite was true in their system.
In the new study, the team relied on optogenetics—a technique that uses light to control neural activity—to artificially activate a set of specific, genetically identified neurons in the lateral septa of mice. During this activation, the mice became more anxious. Moreover, the researchers found that even a brief, transient activation of those neurons could produce a state of anxiety lasting for at least half an hour. This indicates that not only are these cells involved in the initial activation of an anxious state, but also that an anxious state persists even after the neurons are no longer being activated.