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 PsychologyNorthwestern University, Evanston, IL 60208-2710, USA.
American Psychologist (Impact Factor: 6.87). 02/2006; 61(1):10-26. DOI: 10.1037/0003-066X.61.1.10
Source: PubMed

ABSTRACT 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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    • "However, individual differences in intrinsic connectivity may be a pre-existing risk factor for the development of an anxiety disorder. For example, a stress-diathesis approach suggests that anxiety is due to the interaction of risk factors such as sex, genetics, personality (Mineka and Zinbarg 2006), brain structure (Gilbertson et al. 2002) and learning (Caulfield et al. 2013; Holloway et al. 2013; Caulfield et al. 2015). It is likely that connectivity may also play an essential role in mediating risk for developing clinical anxiety. "
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    ABSTRACT: This study characterized cerebellar connectivity with executive intrinsic functional connectivity networks. Using seed regions at the right and left dorsolateral prefrontal cortices (dlPFC) and right orbital frontoinsula, we measured resting-state brain connectivity in healthy college-aged participants. Based on the previous research demonstrating a relationship between the cerebellum and self-report measures of behavioral inhibition, we assessed individual differences in connectivity between groups. Overall, intrinsic activity in cerebellar lobule VIII was significantly correlated with the executive network and cerebellar Crus I with the salience network. Between-group comparisons indicated stronger cerebellar connectivity with the executive network in behaviorally inhibited individuals. Intrinsic activity in Crus I, a region previously implicated in non-motor cerebellar functions, significantly correlated with intrinsic activity in the right dlPFC seed region. These findings support a growing number of studies demonstrating cerebellar influence on higher cognitive processes, extending this relationship to individual differences in anxiety vulnerability.
    Brain Structure and Function 08/2015; DOI:10.1007/s00429-015-1088-6 · 5.62 Impact Factor
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    • "Consequentially, not only exaggerated reactions to threat signals, but also deficits in learning or processing of safety signals can lead to maladaptive fear responses, i.e., responses that are disproportional and/or contextually inappropriate (Mineka and Zinbarg, 2006) or generalize to innocuous stimuli (Dymond et al. 2014). During the past years, the importance for adaptive responding of the latter inhibitory safety learning processes has gained increasing attention (Kong et al. 2014, Pollak et al. 2010), and pathological anxiety has been linked to deficits in inhibitory fear M a n u s c r i p t 4 processing and/or maladaptive stimulus generalization during fear learning (Gazendam et al., 2013; Haddad et al., 2012; Indovina et al., 2011; Kindt and Soeter, 2014), extinction (Gazendam et al., 2013; Sehlmeyer et al., 2011) and return of fear (Kindt et al., 2009; Kindt and Soeter, 2013; Soeter and Kindt, 2010). "
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    ABSTRACT: Impaired fear inhibition has been described as a hallmark of pathological anxiety. We aimed at further characterizing the relation between fear inhibition and anxiety by extending previous work to contextual safety stimuli as well as to dimensional scores of trait anxiety in a large sample. We employed a validated paradigm for context-dependent fear acquisition/extinction (day1) and retrieval/expression (day2) in 377 healthy individuals. This large sample size allowed the employment of a dimensional rather than binary approach with respect to individual differences in trait anxiety. We observed a positive correlation on day 1 between trait anxiety with all CSs that possess an inherent inhibitory component, conveyed either by reliable non-reinforcement of a specific CS in a dangerous context (safe cue) or by the context itself (i.e., safe context). No correlation however was observed for a CS that possesses excitatory (threatening) properties only. These results were observed during fear learning (day 1) for US expectancy and fear ratings but not for SCRs. No such pattern was evident during fear and extinction retrieval/expression (day 2). We provide further evidence that high trait anxiety is associated with the inability to take immediate advantage of environmental safety cues (cued and contextual), which might represent a promising trans-diagnostic marker for different anxiety disorders. Consequently, the incorporation of methods to optimize inhibitory learning in current cognitive behavioral therapy (CBT) treatments might open up a promising avenue for precision medicine in anxiety disorders. We did not include patients diagnosed with anxiety disorders. Copyright © 2015. Published by Elsevier B.V.
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    • "Abnormal or irrational expressions of avoidance are a core feature of anxiety disorders such as separation anxiety disorder, acute stress disorder and posttraumatic stress disorder (PTSD) (American Psychiatric Association, 2013). Neurobiological processes that increase the expression of avoidance or its resistance to extinction represent vulnerabilities to develop anxiety disorders, in keeping with diathesis models of anxiety disorders (Mineka and Zinbarg, 2006). Animal models of avoidance as a means to understand the etiology of anxiety disorders is consistent with recent organizational efforts in psychopathology for research domain criteria (RDoC) (Sanislow et al., 2010). "
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    ABSTRACT: Inbred Wistar Kyoto (WKY) rats express inhibited temperament, increased sensitivity to stress, and exaggerated expressions of avoidance. A long-standing observation for lever press escape/avoidance learning in rats is the duration of the warning signal (WS) determines whether avoidance is expressed over escape. Outbred female Sprague-Dawley (SD) rats trained with a 10-s WS efficiently escaped, but failed to exhibit avoidance; avoidance was exhibited to a high degree with WSs longer than 20-s. We examined this longstanding WS duration function and extended it to male SD and male and female WKY rats. A cross-over design with two WS durations (10 or 60 s) was employed. Rats were trained (20 trials/session) in four phases: acquisition (10 sessions), extinction (10 sessions), re-acquisition (8 sessions) and re-extinction (8 sessions). Consistent with the literature, female and male SD rats failed to express avoidance to an appreciable degree with a 10-s WS. When these rats were switched to a 60-s WS, performance levels in the initial session of training resembled the peak performance of rats trained with a 60-s WS. Therefore, the avoidance relationship was acquired, but not expressed at 10-s WS. Further, poor avoidance at 10-s does not adversely affect expression at 60-s. Failure to express avoidance with a 10-s WS likely reflects contrasting reinforcement value of avoidance, not a reduction in the amount of time available to respond or competing responses. In contrast, WKY rats exhibited robust avoidance with a 10-s WS, which was most apparent in female WKY rats. Exaggerated expression of avoidances by WKY rats, especially female rats, further confirms this inbred strain as a model of anxiety vulnerability.
    Frontiers in Behavioral Neuroscience 07/2015; 9:168. DOI:10.3389/fnbeh.2015.00168 · 3.27 Impact Factor
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