Stress-Induced Anxiety Triggered by Neural Circuitry

stress-induced anxiety

Stress-induced anxiety is apparently triggered by specific neural circuitry, according to new research led by biologists at the California Institute of Technology (Caltech).  These researchers believed that there were clues elsewhere in the brain to indicate how the brain processed anxiety, and their gut instincts paid off.

Traditional studies on stress-induced anxiety have focused on the amygdala, known as the brain’s fear processing center.  While the role of the amygdala isn’t discounted in this current study, it’s been found that there could be another area of the brain that could play a significant role in how the brain processes anxiety.  However, the Caltech biologists believed that the lateral septum (LS) could offer medical professionals some clues as to what potentially triggers anxiety, and in looking at the brains of mice, they were right.

According to the National Institute for Mental Health, up to 18 percent of American adults struggle with anxiety on a daily basis.  In using these mouse models, researchers saw a neural pathway that directly linked the lateral septum to other areas of the brain and influenced how the brain processed anxiety.  Researchers used optogenics, or light to influence neural activity, on mice to see how their brains responded to anxiety.

In working to discover that stress-induced anxiety could be triggered by specific neural circuitry, researchers looked to trigger specific, genetically identified neurons, causing heightened anxiety in mice for up to half an hour.  However, the neurons affected were actually inhibiting neurons.  In other words, the neurons affected should have inhibited or shut down the anxiety response, not allowed the anxiety to rise.

Todd J. Anthony, research fellow at Caltech and David Anderson, Seymour Benzer Professor of Biology at Caltech, were two of the study’s authors.  They said that the research team thought that perhaps these neurons possibly were designed to function as a double inhibitor and would therefore not work to shut the anxiety response down as the researchers anticipated.  In simpler terms, the researchers are working from the philosophy that two negatives make a positive.

Instead of completely shutting down the anxiety response, the affected neurons sent another signal through the brain to the hypothalamus, which had inhibitory neurons affected.  These neurons then sent a signal to the paraventrical nucleus, or PVN, which has become well known as a control point for the release of stress hormones like cortisol.  Cortisol plays a significant role in the stress and anxiety production process, as it’s been shown that high levels of cortisol can have an impact on one’s physical health.

Interestingly, the PVN has been implicated in anxiety studies in the past.  This, coupled with the triggering of the double-inhibitory neurons that was seen in the optogenics study of mice, is suspected to have an amplifying effect on stress-induced anxiety.

While there remains a great deal of work to be done in discovering exactly what these double-inhibitory neurons do, it remains clear that the lateral septum remains the neural pathway that medical professionals and researchers alike will be examining carefully to discover exactly how stress-induced anxiety is triggered.  The outcome of the study will certainly lead to more work with the lateral septum, but what it has ultimately done is give those struggling with daily anxiety disorders some clue as to what could be contributing to their condition.

By Christina St-Jean

Sources:

Caltech

News-Medical.net

Cell

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