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.

Functional topography of serotonergic systems supports the Deakin/Graeff hypothesis of anxiety and affective disorders

“…A clear advantage to having a coordinated behavioral response that increases fear, but reduces panic, is evident in the case of contextual fear. In contexts where a predator has been observed previously, but where the presence or absence (and location) of a predator is uncertain, increased contextual fear (freezing behavior) and inhibition of a flight/escaping behavior is clearly adaptive in order to avoid detection by, or direct confrontation with, a potential predator (Blanchard and Blanchard, 1988; Blanchard and Blanchard, 1989; Graeff, 2011; Graeff and Zangrossi, 2010; McNaughton and Corr, 2004).…”

Intrauterine Exposure to Chronic 22 kHz Sound Affects Inhibitory Avoidance and Serotonergic Parameters in Forebrain Areas of Dams and Rat Offspring

“…The observed effects of 22 kHz sound on ETM inhibitory avoidance and the absence of effect on escape behavior suggest that the neurobiological mechanisms related to anxiety and fear states, respectively, might be distinct. Some author shows that panic attack does not activate HPA axis [54], while the anxiety behavior involves the activation of this axis [24] [55]. As mentioned before, if an aversive sound causes chronic stress in pregnant rats [50] [51], activating the HPA axis and increasing glucocorticoid levels in both maternal and fetal blood, one can hypothesize that it could be one of the mechanisms involved in the effect of 22 kHz sound exposure on inhibitory avoidance.…”

Efectos del estrés sobre los procesos de plasticidad y neurogénesis: una revisión

“…Estos dos momentos del estrés median el denominado síndrome general de adaptación (Selye, 1936(Selye, , 1973. Sin embargo, cuando el estímulo estresor persiste, la activación del HPA es mantenida en el tiempo, en cuyo caso se considerará un fenómeno crónico (Graeff, 2011;Graeff & Zangrossi, 2010).…”