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Vasopressin increases human risky cooperative behavior
Edited by Michael S. Gazzaniga, University of California, Santa Barbara, CA, and approved January 5, 2016 (received for review September 24, 2015)

Significance
Most forms of cooperative behavior take place in a mutually beneficial context where cooperation is risky as its success depends on unknown actions of others. In two pharmacological experiments, we show that intranasal administration of arginine vasopressin (AVP), a hormone that regulates mammalian social behaviors such as monogamy and aggression, increases humans’ tendency to engage in mutually beneficial cooperation. Several control tasks ruled out that AVP’s effects were driven by increased willingness to bare risks in the absence of social context, beliefs about the actions of one’s partner, or altruistic concerns. Our findings provide novel causal evidence for a biological factor underlying cooperation and are in accord with previous findings that cooperation is intrinsically rewarding for humans.
Abstract
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.
Footnotes
↵1C.B. and G.N. contributed equally to this work.
- ↵2To whom correspondence should be addressed. Email: camerer{at}hss.caltech.edu.
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.
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.
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