Fear Conditioning in an Emotion Regulation Context: A Fresh Perspective on the Origins of Anxiety Disorders.

Author(s):  
John P. Forsyth ◽  
Georg H. Eifert ◽  
Velma Barrios
2017 ◽  
Vol 225 (3) ◽  
pp. 200-213 ◽  
Author(s):  
Christian Baumann ◽  
Miriam A. Schiele ◽  
Martin J. Herrmann ◽  
Tina B. Lonsdorf ◽  
Peter Zwanzger ◽  
...  

Abstract. Conditioning and generalization of fear are assumed to play central roles in the pathogenesis of anxiety disorders. Here we investigate the influence of a psychometric anxiety-specific factor on these two processes, thus try to identify a potential risk factor for the development of anxiety disorders. To this end, 126 healthy participants were examined with questionnaires assessing symptoms of anxiety and depression and with a fear conditioning and generalization paradigm. A principal component analysis of the questionnaire data identified two factors representing the constructs anxiety and depression. Variations in fear conditioning and fear generalization were solely associated with the anxiety factor characterized by anxiety sensitivity and agoraphobic cognitions; high-anxious individuals exhibited stronger fear responses (arousal) during conditioning and stronger generalization effects for valence and UCS-expectancy ratings. Thus, the revealed psychometric factor “anxiety” was associated with enhanced fear generalization, an assumed risk factor for anxiety disorders. These results ask for replication with a longitudinal design allowing to examine their predictive validity.


2020 ◽  
Author(s):  
Pooja Palkar ◽  
Eric Hollander

In recent years, advances in the fields of neuroimaging and experimental psychology increased our understanding of the basic mechanisms of classical conditioning and learning, contributing to our knowledge of the neurobiology of anxiety disorders. Research has shown that the amygdala is the cornerstone of fear circuitry and that abnormalities in amygdala pathways can affect the acquisition and expression of fear conditioning. Activation of the amygdala in response to disorder-relevant stimuli has been observed in anxiety disorders. The roles of the hippocampus, nucleus accumbens, periaqueductal gray, and insular and medial prefrontal cortices in response to fear have been identified as well. Neurotransmitters such as serotonin, dopamine, γ-aminobutyric acid, glutamate, and some neurosteroids play an important part in the neurobiology of anxiety disorders. Neuropeptides such as oxytocin, neuropeptide Y, galanin, and cholecystokinin have been shown to modulate stress response. Drugs such as N-methyl-d-aspartate (NMDA) antagonists and blockers of voltage-gated calcium channels in the amygdala are anxiolytic. Fear extinction, which entails new learning of fear inhibition, is the mechanism of effective antianxiety treatments such as d-cycloserine, a partial NMDA agonist. Extinction is thought to occur by the medial prefrontal cortex, which inhibits the lateral amygdala under hippocampal modulation. Harnessing extinction to delink neutral stimuli from aversive responses is an important goal of the psychotherapy and pharmacotherapy of anxiety disorders. Discovery of the role of microRNAs in the etiology of anxiety disorders and their possible utility as targets to treat these disorders is fascinating. In this review, we discuss the neurobiology of anxiety disorders, which will help us better manage them clinically. This review contains 5 figures, 6 tables, and 39 references. Key words: Amygdala, anxiety disorders, neurobiology, fear conditioning, neurocircuitry, neurotransmitters, neuropeptides, neurosteroids, endogenous opioids.


2005 ◽  
Vol 43 (11) ◽  
pp. 1391-1424 ◽  
Author(s):  
Shmuel Lissek ◽  
Alice S. Powers ◽  
Erin B. McClure ◽  
Elizabeth A. Phelps ◽  
Girma Woldehawariat ◽  
...  

CNS Spectrums ◽  
2006 ◽  
Vol 11 (4) ◽  
pp. 248-251 ◽  
Author(s):  
Dan J. Stein ◽  
Hisato Matsunaga

ABSTRACTSpecific phobia is the most prevalent of the anxiety disorders. Although there have been relatively few studies of its psychobiology and pharmacotherapy, there is a rich laboratory of literature on fear conditioning and extinction and a clear evolutionary perspective. Advances in the cognitive-affective neuroscience of fear processing may ultimately lead to new approaches to the clinical management of phobias.


2020 ◽  
Author(s):  
Namita Tanya Padgaonkar ◽  
Jessica Uy ◽  
Samantha DePasque ◽  
Adriana Galván ◽  
Tara Peris

Background: Youth with anxiety disorders struggle with managing emotions relative to peers, but the neural basis of this difference has not been examined. Methods: Youth (Mage=13.6; range=8-17) with (n=37) and without (n=24) anxiety disorders completed a cognitive reappraisal task while undergoing fMRI. Emotional reactivity and regulation, functional activation, and beta-series connectivity were compared across groups. Results: Groups did not differ on emotional reactivity or regulation. However, affect ratings and fronto-limbic activation after viewing aversive imagery (with and without regulation) were higher for anxious youth. Anxious youth did not demonstrate age-dependent changes in regulation, whereas regulation in control youth increased linearly. Stronger amygdala-vmPFC connectivity related to greater anxiety in control youth, but less anxiety in anxious youth. Stronger amygdala-frontal pole connectivity related to worse emotion regulation in control youth, but better emotion regulation in anxious youth. Conclusions: Anxious youth regulate when instructed, but this does not relate to age. Viewing aversive imagery related to heightened negative affect even after reappraisal, accompanied by higher fronto-limbic activation. Emotion dysregulation in youth anxiety disorders may stem from heightened emotionality and potent bottom-up neurobiological responses to aversive stimuli. Findings suggest the importance of treatments focused on both reducing initial emotional reactivity and bolstering regulatory capacity.


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