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Published February 23, 2016 | Supplemental Material + Published
Journal Article Open

Vasopressin increases human risky cooperative behavior


The history of humankind is an epic of cooperation, which is ubiquitous across societies and increasing in scale. Much human cooperation occurs where it is risky to cooperate for mutual benefit because successful cooperation depends on a sufficient level of cooperation by others. Here we show that arginine vasopressin (AVP), a neuropeptide that mediates complex mammalian social behaviors such as pair bonding, social recognition and aggression causally increases humans' willingness to engage in risky, mutually beneficial cooperation. In two double-blind experiments, male participants received either AVP or placebo intranasally and made decisions with financial consequences in the "Stag hunt" cooperation game. AVP increases humans' willingness to cooperate. That increase is not due to an increase in the general willingness to bear risks or to altruistically help others. Using functional brain imaging, we show that, when subjects make the risky Stag choice, AVP down-regulates the BOLD signal in the left dorsolateral prefrontal cortex (dlPFC), a risk-integration region, and increases the left dlPFC functional connectivity with the ventral pallidum, an AVP receptor-rich region previously associated with AVP-mediated social reward processing in mammals. These findings show a previously unidentified causal role for AVP in social approach behavior in humans, as established by animal research.

Additional Information

© 2016 National Academy of Sciences. Edited by Michael S. Gazzaniga, University of California, Santa Barbara, CA, and approved January 5, 2016 (received for review September 24, 2015). Published online before print February 8, 2016, doi: 10.1073/pnas.1518825113. This work was supported by a special grant of the Center for Behavioral Brain Sciences, Magdeburg (to M.H.), Deutsche Forschungsgemeinschaft (DFG) (T.M.), and the Betty and Gordon Moore Foundation (C.F.C. and G.N.). Author contributions: C.B., G.N., C.F.C., S.S., B.V., T.F.M., and M.H. designed research; C.B. performed research; C.B., G.N., C.F.C., B.V., T.F.M., and M.H. contributed new reagents/analytic tools; C.B., G.N., S.S., T.F.M., and M.H. analyzed data; and C.B., G.N., C.F.C., B.V., T.F.M., and M.H. wrote the paper. C.B. and G.N. contributed equally to this work. The authors declare no conflict of interest. This article is a PNAS Direct Submission. This article contains supporting information online at www.pnas.org/lookup/suppl/doi:10.1073/pnas.1518825113/-/DCSupplemental.

Attached Files

Published - PNAS-2016-Brunnlieb-2051-6.pdf

Supplemental Material - pnas.1518825113.sapp.pdf


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