The lifetime risk of suffering from an anxiety disorder is fairly high – around 20%. Unfortunately, however, while the number of patients is substantial, existing therapeutic options are often inadequate. This is partly due to the fact that the brain processes giving rise to anxiety remain poorly understood.
Interestingly for fear – a similar emotion – the brain regions involved are well known, and the interaction of the underlying neuronal circuits is increasingly well understood.
Scientists have now identified neurons in the amygdala – the structure known as the brain's fear center – which can cause anxiety behavior. In addition, they demonstrated that the same cells are also involved in the fear response.
A subpopulation of central amygdala neurons plays a key role in the regulation of anxiety. These cells express a protein kinase called PKCδ, which makes them readily identifiable. On their surface, the neurons have receptors for GABA, a neurotransmitter. "PKCδ neurons are continuously inhibited via the GABA receptor," author says.
"GABA is, as it were, the natural tranquilizer for these cells." In their study, published in Nature Neuroscience, the neurobiologists showed that anxiety behavior is observed as soon as the tranquilizing effect is reduced – i.e. when the amount of GABA receptors is decreased.
The scientists also found an association between fear and sustained anxiety. They showed that, as well as triggering a fear response, a traumatic experience can lead to reduced GABA receptor-mediated inhibition and hence to anxiety states. This could help to explain how a complex anxiety disorder such as post-traumatic stress disorder can be triggered by a fear-inducing event.