Experimental public speaking: Contributions to the understanding of the serotonergic modulation of fear

• Public speaking provokes significant subjective and physiologic response.
• Variation in modelling public speaking can generate different results.
• Public speaking engages the brain regions involved in unconditioned fear response.
• Increase of 5-HT function inhibits the fear induced by public speaking.
• Pharmacological modulation of public speaking resembles the clinical response of panic patients.

Public speaking is widely used as a model of experimental fear and anxiety. This review aimed to evaluate the effects of pharmacological challenges on public speaking responses and their implications for the understanding of the neurobiology of normal and pathological anxiety, specifically panic disorder. We also describe methodological features of experimental paradigms using public speaking as an inducer of fear and stress. Public speaking is a potent stressor that can provoke significant subjective and physiological responses. However, variations in the manners in which public speaking is modelled can lead to different responses that need to be considered when interpreting the results. Results from pharmacological studies with healthy volunteers submitted to simulated public speaking tests have similarities with the pharmacological responses of panic patients observed in clinical practice and panic patients differ from controls in the response to the public speaking test. These data are compatible with the Deakin and Graeff hypothesis that serotonin inhibits fear, as accessed by public speaking tasks, and that this inhibition is likely related to the actions of serotonin in the dorsal periaqueductal grey matter.