Development of anxiety: The role of threat appraisal and fear learning

Mood and Anxiety Disorders Program, National Institute of Mental Health, 9000 Rockville Pike, Bethesda, MD 20892, USA.
Depression and Anxiety (Impact Factor: 4.41). 01/2011; 28(1):5-17. DOI: 10.1002/da.20733
Source: PubMed

ABSTRACT Anxious individuals exhibit threat biases at multiple levels of information processing. From a developmental perspective, abnormal safety learning in childhood may establish threat-related appraisal biases early, which may contribute to chronic disorders in adulthood. This review illustrates how the interface among attention, threat appraisal, and fear learning can generate novel insights for outcome prediction. This review summarizes data on amygdala function, as it relates to learning and attention, highlights the importance of examining threat appraisal, and introduces a novel imaging paradigm to investigate the neural correlates of threat appraisal and threat-sensitivity during extinction recall. This novel paradigm can be used to investigate key questions relevant to prognosis and treatment. Depression and Anxiety, 2011.© 2010 Wiley-Liss, Inc.

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Available from: Daniel S Pine, Sep 28, 2015
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    • "Another bias that is introduced into this loop of decisions and predictions is attentional bias. It is well documented that people with anxiety disorders show enhanced threat detection, persistently pay more attention to these stimuli, and show a bias in threat appraisal (Britton et al. 2011). Although the role of the hippocampus in this attention bias is not clear, such a role does seem consistent with hippocampal function in orienting, attention, and persistence, as discussed above. "
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    • "Furthermore, medial prefrontal cortex represents the biological relevance of a given stimulus and may convey this information to the dorso-lateral prefrontal cortex (Mechias et al., 2010). Amygdala may play a pivotal role in the learning processes related to emotional reactions, fear, and fear extinction (Phelps et al., 2004; Milad et al., 2009; Britton et al., 2011). Secondly, positive functional connectivity was found in PTSD patients between the amygdala and anterior cingulate cortex in response to stimulations related to emotionally traumatic stimuli (Osuch et al., 2008) and during the observation of fearful faces under anxious conditions in healthy subjects (Robinson et al., 2012). "
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    ABSTRACT: Patients with post-traumatic stress disorder (PTSD) tend to misinterpret innocuous stimuli as potential threats, possibly due to a conditioning provoked by traumatic episodes. Previous neuroimaging evidence has shown an abnormal activation of the amygdala and prefrontal cortex in PTSD patients during fear conditioning and extinction. Nevertheless, the effects of a single-type adverse stressor on that circuit remain poorly explored. We tested the hypothesis that a single-type adverse episode is able to affect the prefrontal cortex and amygdala response to conditioned stimuli. To test this hypothesis, fMRI recordings were performed in PTSD patients and trauma-exposed controls during the observation of neutral and negative paired or non-paired pictures with an adverse stimulus by means of a single association. Results showed that left amygdala activation during negative reinforced stimuli was correlated with the score of PTSD clinical scale across all subjects. Furthermore, in the traumatized non-PTSD group, the activation of the dorso-medial prefrontal cortex and bilateral amygdala was lower during the observation of the reinforced (CS(+)) vs non-reinforced pictures (CS(-)) in response to emotionally negative stimuli. This was not the case in the PTSD patients. These results suggest that in PTSD patients, a single-episode conditioning unveils the failure of an inhibitory mechanism moderating the activity of the prefrontal cortex and amygdala in response to adverse and neutral stimuli. Copyright © 2015. Published by Elsevier Inc.
    Brain research bulletin 03/2015; 114. DOI:10.1016/j.brainresbull.2015.03.001 · 2.72 Impact Factor
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    • "Fear and anxiety are activated by threat and the ability to regulate their responses is essential to adaptation and survival. Moreover, an extensive body of work indicates that abnormalities in the detection of threat may lead to pathological fear and anxiety (Lang et al., 2000; Charney, 2004; Green and Phillips, 2004; Blanchard et al., 2011; Britton et al., 2011). Thus, the biology of fear has attracted considerable attention in relation to the causal and modulatory factors linked to normal and exaggerated fear and anxiety states. "
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    ABSTRACT: When prey animals detect the odor of a predator a constellation of fear-related autonomic, endocrine, and behavioral responses rapidly occur to facilitate survival. How olfactory sensory systems process predator odor and channel that information to specific brain circuits is a fundamental issue that is not clearly understood. However, research in the last 15 years has begun to identify some of the essential features of the sensory detection systems and brain structures that underlie predator odor fear. For instance, the main (MOS) and accessory olfactory systems (AOS) detect predator odors and different types of predator odors are sensed by specific receptors located in either the MOS or AOS. However, complex predator chemosignals may be processed by both the MOS and AOS, which complicate our understanding of the specific neural circuits connected directly and indirectly from the MOS and AOS to activate the physiological and behavioral components of unconditioned and conditioned fear. Studies indicate that brain structures including the dorsal periaqueductal gray, paraventricular nucleus of the hypothalamus, and the medial amygdala appear to be broadly involved in predator odor induced autonomic activity and hypothalamic-pituitary-adrenal stress hormone secretion. The medial amygdala also plays a key role in predator odor unconditioned fear behavior and retrieval of contextual fear memory associated with prior predator odor experiences. Other neural structures including the bed nucleus of the stria terminalis and the ventral hippocampus appear prominently involve in predator odor fear behavior. The basolateral amygdala, medial hypothalamic nuclei, and medial prefrontal cortex are also activated by some but not all predator odors. Future research that characterizes how distinct predator odors are uniquely processed in olfactory systems and neural circuits will provide significant insights into the differences of how diverse predator odors activate fear.
    Frontiers in Behavioral Neuroscience 03/2014; 8:72. DOI:10.3389/fnbeh.2014.00072 · 3.27 Impact Factor
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