ANXIETY
February 12, 2014

Anxiety's New Address

An area of the brain believed to calm us down appears to have quite the opposite effect when anxiety strikes.

One of the reasons medications for anxiety are only somewhat useful is that we don’t fully understand how anxiety works in the brain. It’s hard to treat something if you don’t quite know what it is.

Some of the missing pieces behind the basis for anxiety in the brain have now been sketched in by a new study. And, say the authors, their findings mean that better treatments may become possible.

The amygdala is the brain region most often implicated in the stress response. When animals are stressed, their amygdalas light up in brain scans.

The problem, the team discovered, is that the LS cells were actually inhibiting other inhibitory neurons, which had a net positive, or stimulating, effect.

The amygdala is not the only active brain area when anxiety strikes. The lateral septum (LS) is also believed to play a role in the anxiety response. It had been thought by many that the LS dampens the anxiety response — but this new study makes it clear that the LS actually helps trigger anxiety.

When researchers activated the nerve cells in the LS of mice, the mice became anxious. This response persisted for up to half an hour after the nerve cell stimulation was stopped.

The odd thing — and the reason why the LS was believed to reduce anxiety — is that the neurons of the LS are inhibitory neurons, that is, they actually slow down or turn off the cells to which they’re connected. The problem, the California Institute of Technology team discovered, is that the LS cells were actually inhibiting other inhibitory neurons, which had a net positive, or stimulating, effect.

This meant that the LS ultimately activated cells known to play a role in anxiety and which control the release of stress hormones like cortisol. Indeed, looking further into this idea, the team found that activating the LS neurons led to a rise in cortisol.

When the LS cells in stressed animals were silenced, it lowered cortisol levels.

The research probably won’t lead to a drug for anxiety for a while, but finding that a brain area did just the opposite of what it was thought to is a big step in understanding anxiety, and provides an important piece of the puzzle, according author David Anderson.

“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,” he said. “This study opens up a new line of investigation into the brain circuitry that controls anxiety,” Anderson said in a statement.

Effective treatments are sorely needed, Anderson says. Almost one in five people suffers from anxiety disorders, which can cause a variety of mental and physical symptoms which compromise a person’s quality of life.

“It may seem like all that we've done here is dissect a tiny little piece of brain circuitry, but it's a foothold onto a very big mountain. You have to start climbing someplace,” he added.

The study was carried out by a team at the and published in the journal, Cell.

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