@article{HaegeleSchlagenhaufRappetal.2015,
  author    = {Haegele, Claudia and Schlagenhauf, Florian and Rapp, Michael Armin and Sterzer, Philipp and Beck, Anne and Bermpohl, Felix and Stoy, Meline and Stroehle, Andreas and Wittchen, Hans-Ulrich and Dolan, Raymond J. and Heinz, Andreas},
  title     = {Dimensional psychiatry: reward dysfunction and depressive mood across psychiatric disorders},
  series = {Psychopharmacology},
  volume    = {232},
  journal   = {Psychopharmacology},
  number    = {2},
  publisher = {Springer},
  address   = {New York},
  issn      = {0033-3158},
  doi       = {10.1007/s00213-014-3662-7},
  pages     = {331 -- 341},
  year      = {2015},
  abstract  = {A dimensional approach in psychiatry aims to identify core mechanisms of mental disorders across nosological boundaries. We compared anticipation of reward between major psychiatric disorders, and investigated whether reward anticipation is impaired in several mental disorders and whether there is a common psychopathological correlate (negative mood) of such an impairment. During reward anticipation, we observed significant group differences in ventral striatal (VS) activation: patients with schizophrenia, alcohol dependence, and major depression showed significantly less ventral striatal activation compared to healthy controls. Depressive symptoms correlated with dysfunction in reward anticipation regardless of diagnostic entity. There was no significant correlation between anxiety symptoms and VS functional activation. Our findings demonstrate a neurobiological dysfunction related to reward prediction that transcended disorder categories and was related to measures of depressed mood. The findings underline the potential of a dimensional approach in psychiatry and strengthen the hypothesis that neurobiological research in psychiatric disorders can be targeted at core mechanisms that are likely to be implicated in a range of clinical entities.},
  language  = {en}
}
@article{FriedelSchlagenhaufBecketal.2015,
  author    = {Friedel, Eva and Schlagenhauf, Florian and Beck, Anne and Dolan, Raymond J. and Huys, Quentin J. M. and Rapp, Michael Armin and Heinz, Andreas},
  title     = {The effects of life stress and neural learning signals on fluid intelligence},
  series = {European archives of psychiatry and clinical neuroscience : official organ of the German Society for Biological Psychiatry},
  volume    = {265},
  journal   = {European archives of psychiatry and clinical neuroscience : official organ of the German Society for Biological Psychiatry},
  number    = {1},
  publisher = {Springer},
  address   = {Heidelberg},
  issn      = {0940-1334},
  doi       = {10.1007/s00406-014-0519-3},
  pages     = {35 -- 43},
  year      = {2015},
  abstract  = {Fluid intelligence (fluid IQ), defined as the capacity for rapid problem solving and behavioral adaptation, is known to be modulated by learning and experience. Both stressful life events (SLES) and neural correlates of learning [specifically, a key mediator of adaptive learning in the brain, namely the ventral striatal representation of prediction errors (PE)] have been shown to be associated with individual differences in fluid IQ. Here, we examine the interaction between adaptive learning signals (using a well-characterized probabilistic reversal learning task in combination with fMRI) and SLES on fluid IQ measures. We find that the correlation between ventral striatal BOLD PE and fluid IQ, which we have previously reported, is quantitatively modulated by the amount of reported SLES. Thus, after experiencing adversity, basic neuronal learning signatures appear to align more closely with a general measure of flexible learning (fluid IQ), a finding complementing studies on the effects of acute stress on learning. The results suggest that an understanding of the neurobiological correlates of trait variables like fluid IQ needs to take socioemotional influences such as chronic stress into account.},
  language  = {en}
}
@article{DesernoBeckHuysetal.2015,
  author    = {Deserno, Lorenz and Beck, Anne and Huys, Quentin J. M. and Lorenz, Robert C. and Buchert, Ralph and Buchholz, Hans-Georg and Plotkin, Michail and Kumakara, Yoshitaka and Cumming, Paul and Heinze, Hans-Jochen and Grace, Anthony A. and Rapp, Michael Armin and Schlagenhauf, Florian and Heinz, Andreas},
  title     = {Chronic alcohol intake abolishes the relationship between dopamine synthesis capacity and learning signals in the ventral striatum},
  series = {European journal of neuroscience},
  volume    = {41},
  journal   = {European journal of neuroscience},
  number    = {4},
  publisher = {Wiley-Blackwell},
  address   = {Hoboken},
  issn      = {0953-816X},
  doi       = {10.1111/ejn.12802},
  pages     = {477 -- 486},
  year      = {2015},
  abstract  = {Drugs of abuse elicit dopamine release in the ventral striatum, possibly biasing dopamine-driven reinforcement learning towards drug-related reward at the expense of non-drug-related reward. Indeed, in alcohol-dependent patients, reactivity in dopaminergic target areas is shifted from non-drug-related stimuli towards drug-related stimuli. Such hijacked' dopamine signals may impair flexible learning from non-drug-related rewards, and thus promote craving for the drug of abuse. Here, we used functional magnetic resonance imaging to measure ventral striatal activation by reward prediction errors (RPEs) during a probabilistic reversal learning task in recently detoxified alcohol-dependent patients and healthy controls (N=27). All participants also underwent 6-[F-18]fluoro-DOPA positron emission tomography to assess ventral striatal dopamine synthesis capacity. Neither ventral striatal activation by RPEs nor striatal dopamine synthesis capacity differed between groups. However, ventral striatal coding of RPEs correlated inversely with craving in patients. Furthermore, we found a negative correlation between ventral striatal coding of RPEs and dopamine synthesis capacity in healthy controls, but not in alcohol-dependent patients. Moderator analyses showed that the magnitude of the association between dopamine synthesis capacity and RPE coding depended on the amount of chronic, habitual alcohol intake. Despite the relatively small sample size, a power analysis supports the reported results. Using a multimodal imaging approach, this study suggests that dopaminergic modulation of neural learning signals is disrupted in alcohol dependence in proportion to long-term alcohol intake of patients. Alcohol intake may perpetuate itself by interfering with dopaminergic modulation of neural learning signals in the ventral striatum, thus increasing craving for habitual drug intake.},
  language  = {en}
}