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      Alcohol’s effects on emotionally motivated attention, defensive reactivity and subjective anxiety during uncertain threats

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          Abstract

          Developing a better understanding of how and under what circumstances alcohol affects the emotions, cognitions and neural functions that precede and contribute to dangerous behaviors during intoxication may help to reduce their occurrence. Alcohol intoxication has recently been shown to reduce defensive reactivity and anxiety more during uncertain vs certain threat. However, alcohol’s effects on emotionally motivated attention to these threats are unknown. Alcohol may disrupt both affective response to and attentional processing of uncertain threats making intoxicated individuals less able to avoid dangerous and costly behaviors. To test this possibility, we examined the effects of a broad range of blood alcohol concentrations on 96 participants’ sub-cortically mediated defensive reactivity (startle potentiation), retrospective subjective anxiety (self-report) and cortically assessed emotionally motivated attention (probe P3 event related potential) while they experienced visually cued uncertain and certain location electric shock threat. As predicted, alcohol decreased defensive reactivity and subjective anxiety more during uncertain vs certain threat. In a novel finding, alcohol dampened emotionally motivated attention during uncertain but not certain threat. This effect appeared independent of alcohol’s effects on defensive reactivity and subjective anxiety. These results suggest that alcohol intoxication dampens processing of uncertain threats while leaving processing of certain threats intact.

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          Most cited references34

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          Stress revisited: a critical evaluation of the stress concept.

          With the steadily increasing number of publications in the field of stress research it has become evident that the conventional usage of the stress concept bears considerable problems. The use of the term 'stress' to conditions ranging from even the mildest challenging stimulation to severely aversive conditions, is in our view inappropriate. Review of the literature reveals that the physiological 'stress' response to appetitive, rewarding stimuli that are often not considered to be stressors can be as large as the response to negative stimuli. Analysis of the physiological response during exercise supports the view that the magnitude of the neuroendocrine response reflects the metabolic and physiological demands required for behavioural activity. We propose that the term 'stress' should be restricted to conditions where an environmental demand exceeds the natural regulatory capacity of an organism, in particular situations that include unpredictability and uncontrollability. Physiologically, stress seems to be characterized by either the absence of an anticipatory response (unpredictable) or a reduced recovery (uncontrollable) of the neuroendocrine reaction. The consequences of this restricted definition for stress research and the interpretation of results in terms of the adaptive and/or maladaptive nature of the response are discussed. Copyright © 2011 Elsevier Ltd. All rights reserved.
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            The p300: where in the brain is it produced and what does it tell us?

            Intracranial recordings, lesion studies, and the combination of functional imaging with source analysis have produced a solid body of evidence about the generators of the P300 event-related potential. Although it is impossible to square all findings obtained across and within methodologies, a consistent pattern of generators has emerged, with target-related responses in the parietal cortex and the cingulate and novelty-related activations mainly in the inferior parietal and prefrontal regions. Stimulus modality-specific contributions come from the inferior temporal and superior parietal cortex for the visual and from the superior temporal cortex for the auditory modality. The P300 continues to be an important signature of cognitive processes such as attention and working memory and of its dysfunction in neurologic and mental disorders. It is increasingly being investigated as a potential genetic marker of mental disorders. Knowledge about the generators of the P300 will be crucial for a better understanding of its cognitive significance and its continuing clinical application.
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              Phasic vs sustained fear in rats and humans: role of the extended amygdala in fear vs anxiety.

              Data will be reviewed using the acoustic startle reflex in rats and humans based on our attempts to operationally define fear vs anxiety. Although the symptoms of fear and anxiety are very similar, they also differ. Fear is a generally adaptive state of apprehension that begins rapidly and dissipates quickly once the threat is removed (phasic fear). Anxiety is elicited by less specific and less predictable threats, or by those that are physically or psychologically more distant. Thus, anxiety is a more long-lasting state of apprehension (sustained fear). Rodent studies suggest that phasic fear is mediated by the amygdala, which sends outputs to the hypothalamus and brainstem to produce symptoms of fear. Sustained fear is also mediated by the amygdala, which releases corticotropin-releasing factor, a stress hormone that acts on receptors in the bed nucleus of the stria terminalis (BNST), a part of the so-called 'extended amygdala.' The amygdala and BNST send outputs to the same hypothalamic and brainstem targets to produce phasic and sustained fear, respectively. In rats, sustained fear is more sensitive to anxiolytic drugs. In humans, symptoms of clinical anxiety are better detected in sustained rather than phasic fear paradigms.
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                Author and article information

                Journal
                Soc Cogn Affect Neurosci
                Soc Cogn Affect Neurosci
                scan
                Social Cognitive and Affective Neuroscience
                Oxford University Press
                1749-5016
                1749-5024
                November 2017
                27 July 2017
                27 July 2017
                : 12
                : 11
                : 1823-1832
                Affiliations
                [1 ]Department of Psychology, University of Wisconsin–Madison, Madison, WI, USA,
                [2 ]Department of Psychology, University at Buffalo, The State University of New York, Buffalo, NY, USA
                Author notes
                [* ]Correspondence should be addressed to John J. Curtin, Department of Psychology, University of Wisconsin–Madison, 1202 W. Johnson St., Madison, WI 53706, USA. E-mail: jjcurtin@ 123456wisc.edu
                Article
                nsx095
                10.1093/scan/nsx095
                5714195
                28985425
                12c1a250-582b-4759-a6aa-b1ca0eeddd52
                © The Author (2017). Published by Oxford University Press.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 26 April 2017
                : 20 July 2017
                : 24 July 2017
                Page count
                Pages: 10
                Funding
                Funded by: NIH 10.13039/100000002
                Award ID: R01 AA024388
                Categories
                Original Articles

                Neurosciences
                attention,uncertainty,stress,alcohol,threat,anxiety
                Neurosciences
                attention, uncertainty, stress, alcohol, threat, anxiety

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