Genetic and neural correlates of social behavior: the role of Oxytocin.

• Applicant: Dr. Friedericke Yvonne Küpper
• Subject Area: Personality Psychology, Clinical and Medical Psychology, Methodology
• Term: from 2012 to 2015
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 220546703

The biological basis of social behavior as well as of the processing of social stimuli have been studied widely. In this context an important role of the peptide hormone oxytocin has been shown repeatedly, i.a. by means of molecular-genetic associationstudies. One polymorphism in the oxytocin receptor gene, the rs53576, has provided especially promising results. Analyzing the oxytocin receptor alone, however, merely gives information on postsynaptic reactivity of the oxytocin-system without providing information regarding the release of oxytocin. A combination of both informationswithin the frame of gene x gene-interaction studies, however, would provide a far more complete insight into the genetically determined net-activity of the oxytocin-system as a whole as well as its effects on perception and behavior. CD38 regulates the release of oxytocin. Studies in human subjects have shown genetic variations of the CD38 gene to be associated with social behavior, autism as well as basal expression rates of CD38. In this context the single-nucleotide-polymorphism rs3796863 appears to be an especially budding candidate.A combined analysis of both genetic markers appears to be a promising approach to map the net-oxytocin-system activity. The study at hand attempts to use such a combined analysis to further elucidate the effects of the oxytocin-system activity on social aptitude (self-reports) as well as neural correlates of the processing of social stimuli (fMRI). Additionally, the basal CD38 expression-rate will be related to interindividual differences in social aptitude in healthy subjects for the first time.

• DFG Programme: Research Grants
• Participating Persons: Dr. Phillip Grant; Professor Dr. Jürgen Hennig; Dr. Joao Marin; Professor Dr. Rudolf Maria Stark