Mineka S, Zinbarg R. A contemporary learning theory perspective on the etiology of anxiety disorders-It's not what you thought it was. Am Psychol 61: 10-26

Department of Psychology, Northwestern University, Evanston, Illinois, United States
American Psychologist (Impact Factor: 6.87). 02/2006; 61(1):10-26. DOI: 10.1037/0003-066X.61.1.10
Source: PubMed


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.

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    • "Fear conditioning and extinction are considered to provide laboratory analogues for the acquisition of fear and phobias and the subsequent reduction of fear via exposure-based therapy (Field, 2006; Mineka & Zinbarg, 2006). Whereas fear conditioning refers to the acquisition of fear for a Conditioned Stimulus (CS) due to the pairing of the CS with an aversive Unconditioned Stimulus (US), extinction refers to the reduction of conditioned fear through the repeated unreinforced presentation of a CS after the CS-US pairings. "
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    ABSTRACT: Background and Objectives: Repeated exposure to a conditioned stimulus can lead to a reduction of conditioned fear responses towards this stimulus (i.e., extinction). However, this reduction is often fragile and sensitive to contextual changes. In the current study, we investigated whether extinction of fear responses established through verbal threat instructions is also sensitive to contextual changes. We additionally examined whether verbal instructions can strengthen the effects of a context change. Methods: Fifty-two participants were informed that one colored rectangle would be predictive of an electrocutaneous stimulus, while another colored rectangle was instructed to be safe. Half of these participants were additionally informed that this contingency would only hold when the background of the computer screen had a particular color but not when it had another color. After these instructions, the participants went through an unannounced extinction phase that was followed by a context switch. Results: Results indicate that extinguished verbally conditioned fear responses can return after a context switch, although only as indexed by self-reported expectancy ratings. This effect was stronger when participants were told that CS-US contingency would depend on the background color, in which case a return of fear was also observed on physiological measures of fear. Limitations: Extinction was not very pronounced in this study, possibly limiting the extent to which return of fear could be observed on physiological measures. Conclusions: Contextual cues can impact the return of fear established via verbal instructions. Verbal instructions can further strengthen the contextual control of fear.
    Full-text · Article · Jun 2016 · Journal of Behavior Therapy and Experimental Psychiatry
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    • "Anxiety disorders are highly prevalent and costly psychiatric disorders (Gustavsson et al. 2011) which can be studied in the laboratory by using fear conditioning paradigms (Duits et al. 2015; Lissek et al. 2005; Mineka and Zinbarg 2006). Thereby, processes involved in phasic fear and sustained anxiety (Davis et al. 2010) which represent different features of anxiety disorders (Grillon et al. 2006), can be experimentally investigated through cued and contextual conditioning paradigms, respectively. "
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    ABSTRACT: Being a complex phenotype with substantial heritability, anxiety and related phenotypes are characterized by a complex polygenic basis. Thereby, one candidate pathway is neuronal nitric oxide (NO) signaling, and accordingly, rodent studies have identified NO synthase (NOS-I), encoded by NOS1, as a strong molecular candidate for modulating anxiety and hippocampus-dependent learning processes. Using a multi-dimensional and -methodological replication approach, we investigated the impact of a functional promoter polymorphism (NOS1-ex1f-VNTR) on human anxiety-related phenotypes in a total of 1019 healthy controls in five different studies. Homozygous carriers of the NOS1-ex1f short-allele displayed enhanced trait anxiety, worrying and depression scores. Furthermore, short-allele carriers were characterized by increased anxious apprehension during contextual fear conditioning. While autonomous measures (fear-potentiated startle) provided only suggestive evidence for a modulatory role of NOS1-ex1f-VNTR on (contextual) fear conditioning processes, neural activation at the amygdala/anterior hippocampus junction was significantly increased in short-allele carriers during context conditioning. Notably, this could not be attributed to morphological differences. In accordance with data from a plethora of rodent studies, we here provide converging evidence from behavioral, subjective, psychophysiological and neuroimaging studies in large human cohorts that NOS-I plays an important role in anxious apprehension but provide only limited evidence for a role in (contextual) fear conditioning.
    Full-text · Article · Jan 2016 · Social Cognitive and Affective Neuroscience
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    • "Moreover, these disorders are characterized by deficits in fear extinction. This inability to inhibit fear responses is assumed to largely contribute to the maintenance of anxiety disorders (Lissek et al., 2005;Delgado et al., 2006;Mineka and Zinbarg, 2006;Mineka and Oehlberg, 2008), as well as trauma-and stressor-related disorders (e.g.,Ehlers and Clark, 2000;Mineka and Oehlberg, 2008;Cover et al., 2014). PTSD is assumed to be related to and even caused by a failure to consolidate and retrieve memory for fear extinction (Quirk and Mueller, 2008). "
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    ABSTRACT: Fear acquisition and extinction are valid models for the etiology and treatment of anxiety, trauma- and stressor-related disorders. These disorders are assumed to involve aversive learning under acute and/or chronic stress. Importantly, fear conditioning and stress share common neuronal circuits. The stress response involves multiple changes interacting in a time-dependent manner: (a) the fast first-wave stress response (with central actions of noradrenaline, dopamine, serotonin, corticotropin-releasing hormone, plus increased sympathetic tone and peripheral catecholamine release) and (b) the second-wave stress response (with peripheral release of glucocorticoids after activation of the hypothalamus-pituitary-adrenocortical axis). Control of fear during extinction is also sensitive to these stress-response mediators. In the present review, we will thus examine current animal and human data, addressing the role of stress and single stress-response mediators for successful acquisition, consolidation and recall of fear extinction. We report studies using pharmacological manipulations targeting a number of stress-related neurotransmitters and neuromodulators (monoamines, opioids, endocannabinoids, neuropeptide Y, oxytocin, glucocorticoids) and behavioral stress induction. As anxiety, trauma- and stressor-related disorders are more common in women, recent research focuses on female sex hormones and identifies a potential role for estradiol in fear extinction. We will thus summarize animal and human data on the role of estradiol and explore possible interactions with stress or stress-response mediators in extinction. This also aims at identifying time-windows of enhanced (or reduced) sensitivity for fear extinction, and thus also for successful exposure therapy.
    Full-text · Article · Jan 2016 · Frontiers in Behavioral Neuroscience
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