Kosson, D. S., Budhani, S., Nakic, M., Chen, G., Saad, Z. S., Vythilingam, M., et al. (2006). The role of the amygdala and rostral anterior cingulate in encoding expected outcomes during learning. Neuroimage, 29(4), 1161-1172.
Successful passive avoidance learning is thought to require the use of learned stimulus-reinforcement associations to guide decision making [Baxter, M.G., Murray, E.A., 2002. The amygdala and reward. Nature Reviews Neuroscience 3, 563-573]. The current experiment investigated the neural correlates of successful passive avoidance learning in 19 healthy adults. Behaviorally, subjects showed a distinct pattern of performance: early indiscriminate responding to stimuli (pre-criterion performance), followed by relatively rapid learning before a plateau of successful performance (post-criterion performance). Neural responses to post-criterion correct responses were compared with neural responses to both incorrect responses and pre-criterion correct responses. Post-criterion correct responding was associated with increased activation in regions including rostral anterior cingulate, insula, caudate, hippocampal regions, and the amygdala. Published by Elsevier Inc.
Leonardo, E. D., & Hen, R. (2006). Genetics of affective and anxiety disorders. Annual Review of Psychology, 57, 117-137.
The study of the genetics of complex behaviors has evolved dramatically from the days of the nature versus nurture debates that dominated much of the past century. Here we discuss advances in our understanding of the genetics of affective and anxiety disorders. In particular, we highlight our growing understanding of specific gene-environment interactions that occur during critical periods in development, setting the stage for later behavioral phenotypes. We review the recent literature in the field, focusing on recent advances in our understanding of the role of the serotonin system in establishing normal anxiety levels during development. We emphasize the importance of understanding the effect of genetic variation at the level of functional circuits and provide examples from the literature of how such an approach has been exploited to study novel genetic endpoints, including genetically based variation in response to medication, a potentially valuable phenotype that has not received much attention to date.
Mineka, S., & Zinbarg, R. (2006). A contemporary learning theory perspective on the etiology of anxiety disorders - It's not what you thought it was. American Psychologist, 61(1), 10-26.
The authors describe how contemporary learning theory and research provide the basis for perspectives on the etiology and maintenance of anxiety disorders that capture the complexity associated with individual differences in the development and course of these disorders. These insights from modern research on learning overcome the shortcomings of earlier overly simplistic behavioral approaches, which sometimes have been justifiably criticized. The authors show how considerations of early learning histories and temperamental vulnerabilities affect the short- and long-term outcomes of experiences with stressful events. They also demonstrate how contextual variables during and following stressful learning events affect the course of anxiety disorder symptoms once they develop. This range of variables can lead to a rich and nuanced understanding of the etiology and course of anxiety disorders.
[not in handout, see intranet]
Rau, V., DeCola, J. P., & Fanselow, M. S. (2005). Stress-induced enhancement of fear learning: An animal model of posttraumatic stress disorder. Neuroscience and Biobehavioral Reviews, 29(8), 1207-1223.
Fear is an adaptive response that initiates defensive behavior to protect animals and humans from danger. However, anxiety disorders, such as Posttraumatic Stress Disorder (PTSD), can occur when fear is inappropriately regulated. Fear conditioning can be used to study aspects of PTSD, and we have developed a model in which pre-exposure to a stressor of repeated footshock enhances conditional fear responding to a single context-shock pairing. The experiments in this chapter address interpretations of this effect including generalization and summation or fear, inflation, and altered pain sensitivity. The results of these experiments lead to the conclusion that pre-exposure to shock sensitizes conditional fear responding to similar less intense stressors. This sensitization effect resists exposure therapy (extinction) and amnestic (NMDA antagonist) treatment. The pattern predicts why in PTSD patients, mild stressors cause reactions more appropriate for the original traumatic stressor and why new fears are so readily formed in these patients. This model can facilitate the study of neurobiological mechanisms underlying sensitization of responses observed in PTSD. (c) 2005 Elsevier Ltd. All rights reserved.
Roth, W. T., Wilhelm, F. H., & Pettit, D. (2005). Are current theories of panic falsifiable? Psychological Bulletin, 131(2), 171-192.
The authors examine 6 theories of panic attacks as to whether empirical approaches are capable of falsifying them and their heuristic value. The authors conclude that the catastrophic cognitions theory is least falsifiable because of the elusive nature of thoughts but that it has greatly stimulated research and therapy. The vicious circle theory is falsifiable only if the frightening internal sensations are specified. The 3-alarms theory postulates an indeterminate classification of attacks. Hyperventilation theory has been falsified. The suffocation false alarm theory lacks biological parameters that unambiguously index dyspnea or its distinction between anticipatory and panic anxiety. Some correspondences postulated between clinical phenomena and brain areas by the neuroanatomical hypothesis may be falsifiable if panic does not depend on specific thoughts. All these theories have heuristic value, and their unfalsifiable aspects are capable of modification.
[not in handout, see intranet]
Shumake, J., Barrett, D., & Gonzalez-Lima, F. (2005). Behavioral characteristics of rats predisposed to learned helplessness: Reduced reward sensitivity, increased novelty seeking, and persistent fear memories. Behavioural Brain Research, 164(2), 222-230.
The congenitally helpless rat strain, which was selectively bred for increased susceptibility to learned helplessness, may model the predisposition to affective disorders, including depression and post-traumatic stress disorder. Other than the selected trait, the behavior of this strain is not well characterized. In this study, we assessed congenitally helpless rats on several behavioral tests. First, we assessed reward sensitivity by measuring their consumption of a 5% sucrose solution. Next, we assessed exploratory behavior and fearfulness in both a novel and familiar open field, and in a light-dark test. Finally, we assessed fear conditioning by exposing the animals to 4 tone-shock pairs on I day (acquisition) and then presenting 60 tones over the next 2 days (extinction). Compared to normal Sprague-Dawley controls, congenitally helpless rats showed less consumption of the sucrose solution and more exploratory behavior in the novel, but not the familiar, open fields. They also showed less fearfulness in the light-dark test, but more conditioned freezing to the tone predicting shock. Moreover, this freezing was resistant to extinction; congenitally helpless rats not only failed to show a fear decrement during extinction,!, but actually showed increased fear, a phenomenon termed "paradoxical enhancement." Thus, congenitally helpless rats appear to have a behavioral phenotype characterized by reduced sensitivity to reward, increased drive to explore novel environments, and increased propensity to form, and maintain fear-associated memories. This behavioral phenotype is discussed as resembling the personality of humans vulnerable to post-traumatic stress disorder. (c) 2005 Elsevier B.V. All rights reserved.
White, K. S., Brown, T. A., Somers, T. J., & Barlow, D. H. (2006). Avoidance behavior in panic disorder: The moderating influence of perceived control. Behaviour Research and Therapy, 44(1), 147-157.
The relations among anxiety sensitivity, perceived control, and agoraphobia were examined in 239 patients diagnosed with panic disorder (PD). Most patients exhibited agoraphobia accompanying their PD (98% situational avoidance; 90% experiential avoidance; and 80% endorsed interoceptive fear and avoidance). Anxiety sensitivity and perceived emotional control were associated with agoraphobia, and perceived threat control was found to moderate the relationship between anxiety sensitivity and agoraphobia. Lower levels of perceived control were associated with a stronger relationship between anxiety sensitivity and agoraphobia. Results were consistent for self-reported and clinician-rated agoraphobia. Implications for the role of perceived control in agoraphobia development and treatment are discussed. (c) 2005 Elsevier Ltd. All rights reserved.
Wilson, K. A., & Hayward, C. (2005). A prospective evaluation of agoraphobia and depression symptoms following panic attacks in a community sample of adolescents. Journal of Anxiety Disorders, 19(1), 87-103.
In a community sample of high schoolers who experienced their first panic attack, we examined the prospective relationships among pre-panic vulnerabilities, panic attack severity, and post-panic agoraphobia and depression symptoms. Students were evaluated yearly over 4 years to test the following four hypotheses: (1) pre-panic anxiety sensitivity, negative affect, and childhood behavioral inhibition will serve as vulnerabilities that predict agoraphobia and depression symptoms following a panic attack; (2) these vulnerabilities will lead to more severe panic attacks; (3) severe and spontaneous panic attacks will predict subsequent agoraphobia and depressive symptoms; and (4) the interaction between panic severity and vulnerabilities will be associated with worse outcomes following a panic attack. Results supported the first three hypotheses, but no evidence emerged for an interactive effect. Findings are discussed in light of recent modernized classical conditioning models that address factors contributing to development of more severe panic related psychopathology after panic attacks.