Abstract
Although anxiety disorders are the most common of psychiatric diseases with 28% life prevalence (Kessler et al., 2005), the etiology and neurobehavioral mechanisms underlying anxiety are not fully understood. Anxiety has commonly been separated into dimensions of state and trait anxiety (Freud, 1924; Spielberger, 1966). State anxiety constitutes the transitory negative emotions elicited by a stressor whereas trait anxiety refers to the predisposition to react negatively to stressful situations. Twin studies suggest both genetic and environmental contributions to trait anxiety (Lau et al., 2006). In addition, investigations have begun to demonstrate the role of genetic factors in fear conditioning in humans (Hettema et al., 2003; Lonsdorf et al., 2009), suggesting that genetic influences might determine how we learn from stressful experiences. The idea that fear conditioning provides an explanation for the acquisition of anxiety disorders has a long and storied history in psychological science (e.g., Pavlov, 1927; Mineka and Zinbarg, 2006). In the classic view, the evolutionarily adaptive capacity to defensively respond to learned threats can lead to maladaptive behavior. For instance, an anxious individual may learn that a stimulus or situation is threatening, which may then lead to pathological reactions (e.g., phobias and post-traumatic stress disorder). Understanding how humans control learned fear can provide more effective clinical treatments and has spurred numerous investigations into the brain mechanisms underlying fear regulation.
Highlights
Anxiety disorders are the most common of psychiatric diseases with 28% life prevalence (Kessler et al, 2005), the etiology and neurobehavioral mechanisms underlying anxiety are not fully understood
The CS presented in the predictable room evoked phasic amygdala responses that correlated with trait anxiety levels; subjects with high trait anxiety showed stronger amygdala responses to the CS in the predictable room versus the CS in the safe room
The relationship between trait anxiety and amygdala activity has previously been demonstrated during extinction in healthy adults, such that sustained amygdala responses during extinction are correlated with trait anxiety scores (Barrett and Armony, 2009; Sehlmeyer et al, 2010)
Summary
Anxiety disorders are the most common of psychiatric diseases with 28% life prevalence (Kessler et al, 2005), the etiology and neurobehavioral mechanisms underlying anxiety are not fully understood. Since the authors did not control for non-associative phasic responses (e.g., sensitization) within the three contexts, it is not clear whether activity to the CS in the different rooms is a consequence of stronger acquisition per se, or heightened reactivity in general (Lissek et al, 2005).
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