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Sindermann, C.

Publications and source records attributed to Sindermann, C..

2 recordsLinked to original sources

Oxytocin promotes lying for personal gain in a genotype-dependent manner

Society values honesty, since it fosters trust in others. Although we have a strong moral aversion to lying, particularly when it is self-serving, we nevertheless lie quite frequently and the biological basis for this is poorly understood. The hypothalamic neuropeptide oxytocin has been implicated in a number of anti-social as well as pro-social behaviours, including lying to benefit in-group members or in competitive situations. The aim of the present study was to investigate the effects of oxytocin administration on self-serving lying behaviour and possible moderating effects of genetic underpinnings of the oxytocin receptor. A total of 161 adult men participated in a randomized double-blind placebo-controlled between-subject intranasal oxytocin administration (24 International Units) study where self-serving lying was assessed using the die-in-a-cup paradigm. Additionally, contributions of polymorphisms in the oxytocin receptor gene were investigated using a haplotype approach. Results showed that while placebo-treated subjects behaved honestly across three successive rounds, oxytocin administration promoted self-serving lying, particularly in the third / last round and only to a certain degree (not to the maximum). Moreover, this effect of oxytocin was strongest in carriers of the GCG individual haplotype (rs237887-rs2268491-rs2254298) and non-carriers of the GT individual haplotype (rs53576-rs2268498) on the oxytocin receptor gene. Overall our findings demonstrate that oxytocin administration can promote self-serving lying when subjects are given repeated opportunities to lie and that these effects are moderated by genetic underpinnings of the oxytocin receptor.

genetics

Real-time functional connectivity-based neurofeedback of amygdala-frontal pathways reduces anxiety

Deficient emotion regulation and exaggerated anxiety represent a major transdiagnostic psychopathological marker. On the neural level these deficits have been closely linked to impaired, yet treatment-sensitive, prefrontal regulatory control over the amygdala. Gaining direct control over these pathways could therefore provide an innovative and promising strategy to regulate exaggerated anxiety. To this end the current proof-of-concept study evaluated the feasibility, functional relevance and maintenance of a novel connectivity-informed real-time fMRI neurofeedback training. In a randomized within-subject sham-controlled design high anxious subjects (n = 26) underwent real-time fMRI-guided training to enhance connectivity between the ventrolateral prefrontal cortex (vlPFC) and the amygdala (target pathway) during threat exposure. Maintenance of regulatory control was assessed after three days and in the absence of feedback. Training-induced changes in functional connectivity of the target pathway and anxiety ratings served as primary outcomes. Training of the target, yet not the sham-control, pathway significantly increased amygdala-vlPFC connectivity and decreased subjective anxiety levels. On the individual level stronger connectivity increases were significantly associated with anxiety reduction. At follow-up, volitional control over the target pathway and decreased anxiety level were maintained in the absence of feedback. The present results demonstrate for the first time that successful self-regulation of amygdala-prefrontal top-down regulatory circuits may represent a novel strategy to control anxiety. As such, the present findings underscore both the critical contribution of amygdala-prefrontal circuits to emotion regulation and the therapeutic potential of connectivity-informed real-time neurofeedback.

clinical trials