There is a high level of co-morbidity among those with mental health and substance use…
Neural Contributors to Anxiety
From getting out the door on time to dealing with a hot-headed coworker, people deal with stress every day. Most handle the difficulty and move on, but 18 percent of Americans become panicked. A recent provides new information about the causes of anxiety.
Researchers at the California Institute of Technology (Caltech) began their study with a belief that there could be a neural circuitry problem that contributed to the development of anxiety, and that belief turned out to be proven in the findings.
There is a large body of research documenting the role of the amygdala, the brain’s fear processing center, in anxiety development. But the Caltech researchers wanted to look at the lateral septum (LS), also believed to play a part in triggering anxiety. The researchers used animal models to test their theory. Using animal models the researchers were able to examine how the neural pathway from the lateral septum affected other areas of the brain, including the areas that process anxiety.
The researchers used a technique called optogenics, which uses light to manipulate neural activity, in mice to study how their brains reacted to anxiety. The researchers attempted to trigger specific neurons in an effort to increase anxiety in the mice for up to one half-hour.
Instead, the researchers found that the neurons they affected served to inhibit neurons. While the neurons affected should have shut down the anxiety response, they instead caused the anxiety levels to increase. This was surprising, given that the neurons were expected to shut down the anxiety response.
The authors believed the neurons may have been designed as a way for the brain to use as a double inhibitor and would work to not limit the anxiety response. In other words, they believed the neurons may work in ways best described in mathematical terms: two negatives make a positive.
But instead of limiting the anxiety response the neurons instead sent an additional signal to the hypothalamus, where inhibitory neurons are affected. The neurons then sent a message to the paraventrical nucleus, which governs the release of stress hormones like cortisol. Cortisol is an important contributor to the experience of stress and anxiety, and high levels of the hormone can negatively impact physical health.
The study is not the first to link anxiety to activity in the paraventrical nucleus. The role of the paraventrical nucleus, combined with the double-inhibitory neurons observed in the study, could explain much of the activity related to stress-induced anxiety that takes place in the brain.
The study is likely to lead to more research on anxiety and its relationship to the lateral septum. The impact of the study may not have immediate clinical implications, but it broadens experts’ understanding of the brain processes surrounding anxiety. Eventually it may allow for more effective treatment through medications or other therapies that will improve based on the full knowledge of the brain processes involved.