Variation in the oxytocin receptor gene is associated with pair-bonding and social behavior.

Walum H, Lichtenstein P, Neiderhiser JM, Reiss D, Ganiban JM, Spotts EL, Pedersen NL, Anckars├Ąter H, Larsson H, Westberg L

Biol. Psychiatry 71 (5) 419-426 [2012-03-01; online 2011-10-22]

In specific vole and primate species the neuropeptide oxytocin plays a central role in the regulation of pair-bonding behavior. Here we investigate the extent to which genetic variants in the oxytocin receptor gene (OXTR) are associated with pair-bonding and related social behaviors in humans. We first genotyped twelve single nucleotide polymorphisms (SNPs) in the TOSS (Twin and Offspring Study in Sweden) (n = 2309) and the TCHAD (Swedish Twin Study of Child and Adolescent Development) (n = 1240), comprising measures of self-reported pair-bonding behavior. In the TOSS sample we further investigated one of the SNPs for measures of marital status and quality. Moreover, in the TCHAD sample we explored the longitudinal relationship between precursors of pair-bonding during childhood and subsequent behavior in romantic relationships. Finally, in the TCHAD study and in the Child and Adolescent Twin Study of Sweden (CATSS) (n = 1771), the association between the same SNP and childhood behaviors was investigated. One SNP (rs7632287) in OXTR was associated with traits reflecting pair-bonding in women in the TOSS and TCHAD samples. In girls the rs7632287 SNP was further associated with childhood social problems, which longitudinally predicted pair-bonding behavior in the TCHAD sample. This association was replicated in the CATSS sample in which an association between the same SNP and social interaction deficit symptoms from the autism spectrum was detected. These results suggest an association between variation in OXTR and human pair-bonding and other social behaviors, possibly indicating that the well-described influence of oxytocin on affiliative behavior in voles could also be of importance for humans.

Mutation Analysis Facility (MAF)

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PubMed 22015110

DOI 10.1016/j.biopsych.2011.09.002

Crossref 10.1016/j.biopsych.2011.09.002

mid NIHMS325804

S0006-3223(11)00860-2

pmc PMC3266986