Department of Neuroscience and Behavior, Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.
Institute of Behavioral Neuroscience (INeC), University of São Paulo, Ribeirão Preto, SP, Brazil; Neurobiology of Emotion Research Center (NuPNE), University of São Paulo, Ribeirão Preto, SP, Brazil.
Neurosci Biobehav Rev. 2014 Oct;46 Pt 3:407-17. doi: 10.1016/j.neubiorev.2014.09.011. Epub 2014 Sep 30.
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.
公开演讲被广泛用作实验性恐惧和焦虑的模型。本综述旨在评估药理学挑战对公开演讲反应的影响，以及其对正常和病理性焦虑（特别是恐慌症）神经生物学的理解的影响。我们还描述了使用公开演讲作为恐惧和压力诱导物的实验范式的方法学特征。公开演讲是一种强有力的应激源，可以引起显著的主观和生理反应。然而，公开演讲的模拟方式的变化可能导致不同的反应，在解释结果时需要考虑这些反应。在接受模拟公开演讲测试的健康志愿者中进行的药理学研究结果与在临床实践中观察到的恐慌症患者的药理学反应相似，并且恐慌症患者在对公开演讲测试的反应方面与对照组不同。这些数据与 Deakin 和 Graeff 的假设一致，即 5-羟色胺抑制通过公开演讲任务获得的恐惧，并且这种抑制可能与 5-羟色胺在背侧穹窿周围灰质中的作用有关。
