Defense-related emotions in humans.

Abstract

The study of the role of serotonin in anxiety has led to the view that this neurotransmitter enhances anxiety, but inhibits panic. Validation of this hypothesis has been made using two experimental procedures that increase anxiety in human volunteers. One is classical conditioning of the skin electrical conductance response, which is assumed to represent anxiety. The other is simulated public speaking, which is believed to mobilize the same neural networks that are operative in panic and social anxiety disorders. In general, the results of these studies have fulfilled the predictions derived from the above hypothesis. The same procedures have been applied to panic disorder patients, and the obtained results have shown that these patients had a blunted anxiety response to public speaking. This speaking stress also did not activate the hypothalamic-pituitary-adrenal axis, which, in contrast, was activated by anticipatory anxiety. It may be concluded that anxiety and panic are qualitatively different emotional states, respectively related to the animal defense reactions to potential and proximal threat. In agreement, reported results of recent neuroimaging studies have shown that anxiety activates prefrontal cortical areas, whereas panic activates midbrain regions, particularly the periaqueductal gray matter. As a general conclusion, it may be said that anxiety, fear and panic do not belong to the same continuum of increasing intensity; instead, they are qualitatively different emotional states.