Characterizing the nature of emotional-associative learning deficits in panic disorder: An fMRI study on fear conditioning, extinction training and recall

AbstractIndividuals, who score high in self-reported intolerance of uncertainty (IU), tend to find uncertainty anxiety-provoking. IU has been reliably associated with disrupted threat extinction. However, it remains unclear whether IU would be related to disrupted extinction to other arousing stimuli that are not threatening (i.e., rewarding). We addressed this question by conducting a reward associative learning task with acquisition and extinction training phases (n = 58). Throughout the associative learning task, we recorded valence ratings (i.e. liking), skin conductance response (SCR) (i.e. sweating), and corrugator supercilii activity (i.e. brow muscle indicative or negative and positive affect) to learned reward and neutral cues. During acquisition training with partial reward reinforcement, higher IU was associated with greater corrugator supercilii activity to neutral compared to reward cues. IU was not related to valence ratings or SCR’s during the acquisition or extinction training phases. These preliminary results suggest that IU-related deficits during extinction may be limited to situations with threat. The findings further our conceptual understanding of IU’s role in the associative learning and extinction of reward, and in relation to the processing of threat and reward more generally.

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Effects of intolerance of uncertainty on subjective and psychophysiological measures during fear acquisition and delayed extinction

10.31234/osf.io/hj5gt ◽

2021 ◽

Author(s):

Maren Klingelhöfer-Jens ◽

Jayne Morriss ◽

Tina B Lonsdorf

Keyword(s):

Fear Conditioning ◽

Skin Conductance ◽

Intolerance Of Uncertainty ◽

Acquisition Training ◽

Extinction Training ◽

Future Directions ◽

Psychophysiological Measures ◽

Learned Fear ◽

Startle Blink

Individuals who score high in self-reported Intolerance of Uncertainty (IU) tend to find uncertainty unacceptable and aversive. In recent years, research has shed light on the role of IU in modulating subjective (i.e. expectancy ratings) and psychophysiological responses (i.e. skin conductance) across different classical fear conditioning procedures, particularly that of immediate extinction. However, there remain gaps in understanding how IU, in comparison to other negative emotionality traits (STAI-T), impact different types of subjective and psychophysiological measures during different classical fear conditioning procedures. Here, we analyzed IU, STAI-T, subjective (i.e. fear ratings) and psychophysiological (i.e. skin conductance, auditory startle blink) data recorded during fear acquisition training and 24h-delayed extinction training (n = 66). Higher IU, over STAI-T, was: (1) significantly associated with greater fear ratings to the learned fear cue during fear acquisition training, and (2) at trend associated with greater fear ratings to the learned fear versus safe cue during delayed extinction training. Both IU and STAI-T were not related to skin conductance or auditory startle blink during fear acquisition training and delayed extinction training. These results add to and extend our current understanding of the role of IU on subjective and physiological measures during different fear conditioning procedures, particularly that of delayed extinction training. Implications of these findings and future directions are discussed.

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Neonatal Exposure to Sevoflurane Induces Abnormal Social Behaviors and Deficits in Fear Conditioning in Mice

Anesthesiology ◽

10.1097/aln.0b013e3181974fa2 ◽

2009 ◽

Vol 110 (3) ◽

pp. 628-637 ◽

Cited By ~ 307

Author(s):

Maiko Satomoto ◽

Yasushi Satoh ◽

Katsuo Terui ◽

Hideki Miyao ◽

Kunio Takishima ◽

...

Keyword(s):

Social Interaction ◽

Social Behavior ◽

Fear Conditioning ◽

Social Behaviors ◽

Autism Spectrum ◽

Social Recognition ◽

Neonatal Exposure ◽

Learning Deficits ◽

Neonatal Mice ◽

The Social

Background Neonatal exposure to anesthetics that block N-methyl-D-aspartate receptors and/or hyperactivate gamma-aminobutyric acid type A receptor has been shown to cause neuronal degeneration in the developing brain, leading to functional deficits later in adulthood. The authors investigated whether exposure of neonatal mice to inhaled sevoflurane causes deficits in social behavior as well as learning disabilities. Methods Six-day-old C57BL/6 mice were exposed to 3% sevoflurane for 6 h. Activated cleaved caspase-3 immunohistochemical staining was used for detection of apoptosis. Cognitive functions were tested by pavlovian conditioned fear test. Social behavior was tested by social recognition and interaction tests. Results Neonatal exposure to sevoflurane significantly increased the number of apoptotic cells in the brain immediately after anesthesia. It caused persistent learning deficits later in adulthood as evidenced by decreased freezing response in both contextual and cued fear conditioning. The social recognition test demonstrated that mice with neonatal exposure to sevoflurane did not develop social memory. Furthermore, these mice showed decreased interactions with a social target compared with controls in the social interaction test, indicating a social interaction deficit. The authors did not attribute these abnormalities in social behavior to impairments of general interest in novelty or olfactory sensation, because they did not detect significant differences in the test for novel inanimate object interaction or for olfaction. Conclusions This study shows that exposure of neonatal mice to inhaled sevoflurane could cause not only learning deficits but also abnormal social behaviors resembling autism spectrum disorder.

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Prefrontal cortical contributions during discriminative fear conditioning, extinction, and spontaneous recovery in rats

Experimental Brain Research ◽

10.1007/s00221-010-2228-0 ◽

2010 ◽

Vol 203 (2) ◽

pp. 285-297 ◽

Cited By ~ 44

Author(s):

Erin L. Zelinski ◽

Nancy S. Hong ◽

Amanda V. Tyndall ◽

Brett Halsall ◽

Robert J. McDonald

Keyword(s):

Fear Conditioning ◽

Spontaneous Recovery ◽

Prefrontal Cortical ◽

Discriminative Fear Conditioning ◽

Conditioning Extinction

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Fear conditioning in panic disorder: Enhanced resistance to extinction.

Journal of Abnormal Psychology ◽

10.1037/0021-843x.116.3.612 ◽

2007 ◽

Vol 116 (3) ◽

pp. 612-617 ◽

Cited By ~ 139

Author(s):

Tanja Michael ◽

Jens Blechert ◽

Noortje Vriends ◽

Jürgen Margraf ◽

Frank H. Wilhelm

Keyword(s):

Panic Disorder ◽

Fear Conditioning ◽

Resistance To Extinction ◽

Enhanced Resistance

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The Neurobiological Basis of Anxiety and Fear: Circuits, Mechanisms, and Neurochemical Interactions (Part II)

The Neuroscientist ◽

10.1177/107385849800400208 ◽

1998 ◽

Vol 4 (2) ◽

pp. 122-132 ◽

Cited By ~ 12

Author(s):

Dennis S. Charney ◽

Christian C. G. Grillon ◽

J. Douglas Bremner

Keyword(s):

Posttraumatic Stress Disorder ◽

Panic Disorder ◽

Behavioral Sensitization ◽

Stress Disorder ◽

Signs And Symptoms ◽

Brain Structures ◽

Neural Mechanisms ◽

Cortical Regions ◽

Anxiety And Fear ◽

Conditioning Extinction

This article is Part II of a review of the neuronal circuits, neural mechanisms, and neuromodulators that seem to be involved in anxiety and fear states. Part I focused on the specific brain structures, including the roles of the amygdala, locus coeruleus, hippocampus, and various cortical regions and the neural mechanisms of fear conditioning, extinction, and behavioral sensitization in mediating the signs and symptoms of anxiety and fear. Part II attempts to develop a better understanding of neurochemical mediation of traumatic remembrance and the neurobiological consequences of stress, particularly when experienced early in life. Finally, the data is synthesized to provide a basis for understanding the pathophysiology of anxiety disorders, such as Panic disorder and Posttraumatic Stress Disorder. NEUROSCIENTIST 4:122–132, 1998

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