@article{HodappRabovsky2021,
  author    = {Hodapp, Alice and Rabovsky, Milena},
  title     = {The N400 ERP component reflects an error-based implicit learning signal during language comprehension},
  series = {European journal of neuroscience},
  volume    = {54},
  journal   = {European journal of neuroscience},
  number    = {9},
  publisher = {Wiley},
  address   = {Oxford},
  issn      = {0953-816X},
  doi       = {10.1111/ejn.15462},
  pages     = {7125 -- 7140},
  year      = {2021},
  abstract  = {The functional significance of the N400 evoked-response component is still actively debated. An increasing amount of theoretical and computational modelling work is built on the interpretation of the N400 as a prediction error. In neural network modelling work, it was proposed that the N400 component can be interpreted as the change in a probabilistic representation of meaning that drives the continuous adaptation of an internal model of the statistics of the environment. These results imply that increased N400 amplitudes should correspond to greater adaptation, which can be measured via implicit memory. To investigate this model derived hypothesis, the current study manipulated expectancy in a sentence reading task to influence N400 amplitudes and subsequently presented the previously expected vs. unexpected words in a perceptual identification task to measure implicit memory. As predicted, reaction times in the perceptual identification task were significantly faster for previously unexpected words that induced larger N400 amplitudes in the previous sentence reading task. Additionally, it could be demonstrated that this adaptation seems to specifically depend on the process underlying N400 amplitudes, as participants with larger N400 differences during sentence reading also exhibited a larger implicit memory benefit in the perceptual identification task. These findings support the interpretation of the N400 as an implicit learning signal driving adaptation in language processing.},
  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}
}