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      A Preliminary Study of DBH (Encoding Dopamine Beta-Hydroxylase) Genetic Variation and Neural Correlates of Emotional and Motivational Processing in Individuals With and Without Pathological Gambling

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          Abstract

          Background and aims

          Corticostriatal-limbic neurocircuitry, emotional and motivational processing, dopaminergic and noradrenergic systems and genetic factors have all been implicated in pathological gambling (PG). However, allelic variants of genes influencing dopaminergic and noradrenergic neurotransmitters have not been investigated with respect to the neural correlates of emotional and motivational states in PG. Dopamine beta-hydroxylase (DBH) converts dopamine to norepinephrine; the T allele of a functional single-nucleotide polymorphism rs1611115 (C-1021T) in the DBH gene is associated with less DBH activity and has been linked to emotional processes and addiction. Here, we investigate the influence of rs1611115 on the neural correlates of emotional and motivational processing in PG and healthy comparison (HC) participants.

          Methods

          While undergoing functional magnetic resonance imaging, 18 PG and 25 HC participants, all European Americans, viewed gambling-, sad-, and cocaine-related videotapes. Analyses focused on brain activation differences related to DBH genotype (CC/T-carrier [i.e., CT and TT]) and condition (sad/gambling/cocaine).

          Results

          CC participants demonstrated greater recruitment of corticostriatal-limbic regions, relative to T-carriers. DBH variants were also associated with altered corticostriatal-limbic activations across the different videotape conditions, and this association appeared to be driven by greater activation in CC participants relative to T-carriers during the sad condition. CC relative to T-carrier subjects also reported greater subjective sadness to the sad videotapes.

          Conclusions

          Individual differences in genetic composition linked to aminergic function contribute significantly to emotional regulation across diagnostic groups and warrant further investigation in PG.

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          Most cited references 50

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          Dysfunction of the prefrontal cortex in addiction: neuroimaging findings and clinical implications.

          The loss of control over drug intake that occurs in addiction was initially believed to result from disruption of subcortical reward circuits. However, imaging studies in addictive behaviours have identified a key involvement of the prefrontal cortex (PFC) both through its regulation of limbic reward regions and its involvement in higher-order executive function (for example, self-control, salience attribution and awareness). This Review focuses on functional neuroimaging studies conducted in the past decade that have expanded our understanding of the involvement of the PFC in drug addiction. Disruption of the PFC in addiction underlies not only compulsive drug taking but also accounts for the disadvantageous behaviours that are associated with addiction and the erosion of free will.
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            Amygdala and ventromedial prefrontal cortex are inversely coupled during regulation of negative affect and predict the diurnal pattern of cortisol secretion among older adults.

            Among younger adults, the ability to willfully regulate negative affect, enabling effective responses to stressful experiences, engages regions of prefrontal cortex (PFC) and the amygdala. Because regions of PFC and the amygdala are known to influence the hypothalamic-pituitary-adrenal axis, here we test whether PFC and amygdala responses during emotion regulation predict the diurnal pattern of salivary cortisol secretion. We also test whether PFC and amygdala regions are engaged during emotion regulation in older (62- to 64-year-old) rather than younger individuals. We measured brain activity using functional magnetic resonance imaging as participants regulated (increased or decreased) their affective responses or attended to negative picture stimuli. We also collected saliva samples for 1 week at home for cortisol assay. Consistent with previous work in younger samples, increasing negative affect resulted in ventral lateral, dorsolateral, and dorsomedial regions of PFC and amygdala activation. In contrast to previous work, decreasing negative affect did not produce the predicted robust pattern of higher PFC and lower amygdala activation. Individuals demonstrating the predicted effect (decrease < attend in the amygdala), however, exhibited higher signal in ventromedial prefrontal cortex (VMPFC) for the same contrast. Furthermore, participants displaying higher VMPFC and lower amygdala signal when decreasing compared with the attention control condition evidenced steeper, more normative declines in cortisol over the course of the day. Individual differences yielded the predicted link between brain function while reducing negative affect in the laboratory and diurnal regulation of endocrine activity in the home environment.
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              Dopaminergic network differences in human impulsivity.

              Dopamine (DA) has long been implicated in impulsivity, but the precise mechanisms linking human variability in DA signaling to differences in impulsive traits remain largely unknown. By using a dual-scan positron emission tomography approach in healthy human volunteers with amphetamine and the D2/D3 ligand [18F]fallypride, we found that higher levels of trait impulsivity were predicted by diminished midbrain D2/D3 autoreceptor binding and greater amphetamine-induced DA release in the striatum, which was in turn associated with stimulant craving. Path analysis confirmed that the impact of decreased midbrain D2/D3 autoreceptor availability on trait impulsivity is mediated in part through its effect on stimulated striatal DA release.
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                Author and article information

                Journal
                jba
                JBA
                Journal of Behavioral Addictions
                J Behav Addict
                Akadémiai Kiadó (Budapest )
                2062-5871
                2063-5303
                19 May 2016
                June 2016
                : 5
                : 2
                : 282-292
                Affiliations
                [1 ]Department of Psychiatry, Yale University School of Medicine , New Haven, CT, USA
                [2 ]Department of Diagnostic Radiology, Yale University School of Medicine , New Haven, CT, USA
                [3 ]Child Study Center, Yale University School of Medicine , New Haven, CT, USA
                [4 ]Department of Neuroscience, Yale University School of Medicine , New Haven, CT, USA
                [5 ]CASAColumbia, Yale University School of Medicine , New Haven, CT, USA
                [6 ] Connecticut Mental Health Center , New Haven, CT, USA
                Author notes
                [* ]Corresponding author: Marc N. Potenza, MD, PhD; Connecticut Mental Health Center, Room S-104, 34 Park Street, New Haven, CT 06519, USA; Phone: +1 203 974 7365; Fax: +1 203 974 7366; E-mail: marc.potenza@ 123456yale.edu
                Article
                10.1556/2006.5.2016.026
                5387779
                27194378
                © 2016 The Author(s)

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium for non-commercial purposes, provided the original author and source are credited.

                Page count
                Figures: 2, Tables: 3, Equations: 0, References: 45, Pages: 11
                Funding
                Funding sources: Funding was provided by NIH grants K01 DA24758, R01 DA019039, R01 DA012849, R01 DA012690, R01 DA018647, P20 DA027844, CASAColumbia, a Brain and Behavior Research NARSAD Young Investigator award, the Connecticut State Department of Mental Health and Addictions Services, the Connecticut Mental Health Center, an unrestricted research gift from the Mohegan Sun Casino, and the Yale Gambling Center of Research Excellence Award grant from the National Center for Responsible Gaming. The funding agencies did not provide input or comment on the content of the manuscript, and the content of the manuscript reflects the contributions and thoughts of the authors and do not necessarily reflect the views of the funding agencies.
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