Klucken, Tim
Preferred name
Klucken, Tim
Email
tim.klucken@uni-siegen.de
ORCID
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Publication Access status: Open Access , Failure to replicate the association between fractional anisotropy and the serotonin transporter gene (5-HTTLPR, rs25531)Recent work underlines the importance of alterations in white matter (e.g., measured by fractional anisotropy (FA)) as a neural vulnerability marker for psychiatric disorders. In this context, the uncinate fasciculus (UF), which connects the limbic system with prefrontal areas, has repeatedly been linked to psychiatric disorders, fear processing, and anxietyrelated traits. Individual differences in FA may partly be genetically determined. Variation in the promoter region of the serotonin transporter gene (serotonin transporter-linked polymorphic region [5-HTTLPR]) is a particularly promising candidate in this context, which has been linked to psychiatric disorders as well as to limbic and prefrontal reactivity. However, findings on the association between the 5-HTTLPR and FA within the UF-tract have been heterogeneous. The present study investigated this relationship and extended previous work by considering different genetic classification approaches as well as sex effects in a human sample (n = 114). All participants were genotyped for the 5-HTTLPR and the rs25531 polymorphism. As a main result, we did not find any significant relationship between the 5-HTTLPR and FA in the UF-tract although power analyses showed an adequate power. In addition, genotype effects were neither found when different classification approaches were used nor when analyses were carried out in males or females only. The present findings suggest that the association of the 5-HTTLPR and FA seems to be a more labile phenomenon than previously assumed. Possible explanations and limitations are discussed.Source Type:Article596 249 - Some of the metrics are blocked by yourconsent settings
Publication Access status: Open Access , Relationship of sensation seeking with the neural correlates of appetitive conditioningPrevious research has linked sensation seeking with a heightened risk for drug abuse and other risk-taking behavior. As appetitive conditioning presents a model for the etiology and maintenance of addictive behavior, investigating sensation seeking in a classical conditioning paradigm might elucidate possible pathways toward addiction within this model. Furthermore, the theoretical concept underlying sensation seeking proposes a negative relationship between reward processing and sensation seeking in only moderately arousing situations, which has been neglected by previous research. This study aimed to investigate this inverse relationship in moderately stimulating situations entailing reward processing using functional magnetic resonance imaging. Subjects (N = 38) participated in a classical conditioning paradigm in which a neutral stimulus (CS+) was repeatedly paired with a monetary reward, while another neutral stimulus (CS−) was not. Imaging results revealed a negative relationship between sensation seeking and neural responses in the insula, amygdala and nucleus accumbens during the early phase and in the dorsal anterior cingulate cortex during the late phase of conditioning. These findings suggest reduced reward learning and consequently diminished processing of outcome expectancy in appetitive conditioning in subjects with high sensation seeking scores. The results are discussed with respect to clinical implications.Source Type:Article319 138 - Some of the metrics are blocked by yourconsent settings
Publication Access status: Open Access , Retraining automatic action tendencies for smoking using mobile phone-based approach-avoidance bias training: a study protocol for a randomized controlled studyBackground Automatic tendencies to approach drug-related cues have been linked to the development and maintainance of harmful drug-taking behavior. Recent studies have demonstrated that these automatic approach tendencies can be targeted directly by means of cognitive bias modification (CBM). Moreover, changing those approach tendencies may enhance treatment outcomes. However, training and therapy effects tend to be rather small and adherence to the training might be impaired by time-consuming multiple laboratory training sessions. Here, we present a protocol for a randomized controlled design to improve CBM training efficiency and facilitate access to the training by providing mobile-phone-based training sessions at home to current smokers motivated to quit smoking. Methods Participants (n = 100) are current smokers who smoke at least six cigarettes per day for at least 6 months and are willing to quit smoking. All participants attend a brief behavioral smoking cessation intervention (TAU) and are randomly assigned either to an experimental (TAU + training) or a control group. Participants in the experimental condition are given access to a training application (app) aimed at retraining automatic approach biases for smoking cues. Participants are instructed to perform the app training outside the laboratory context on a daily basis for 14 consecutive days. Participants in the control group do not receive the training. Primary outcome measures are changes in smoking-related approach biases and reductions in daily nicotine consumption as assessed at baseline, post-training and at 6-week follow up. Secondary outcome measures include approach biases for alternative stimuli or smoking stimuli to which participants were not exposed during training, attentional and association biases, biochemical outcomes, and self-reported smoking behavior, also measured at three different time points (baseline, post-training, and follow up). After completion of the study, smokers in the control condition will receive access to the training app. Discussion This randomized controlled trial is the first to test the effectiveness of an app-based CBM intervention as an adjunct to a brief smoking cessation intervention in smokers motivated to quit smoking. The results of this study can inform future research in the optimization and advancement of CBM treatment for addiction.Source Type:Article465 115