1. Center for Behavioral Neuroscience and Department of Psychiatry and Behavioral Sciences, Emory University, Atlanta, Georgia 30322, USA
2. Department of Psychology and Neuroscience Program, Florida State University, Tallahassee, Florida 32306, USA
3. Harvard Institutes of Medicine and Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA

Correspondence to: Larry J. Young¹ Email: lyoun03@emory.edu

The molecular mechanisms underlying the evolution of complex behaviour are poorly understood. The mammalian genus Microtus provides an excellent model for investigating the evolution of social behaviour. Prairie voles (Microtus ochrogaster) exhibit a monogamous social structure in nature, whereas closely related meadow voles (Microtus pennsylvanicus) are solitary and polygamous¹. In male prairie voles, both vasopressin and dopamine act in the ventral forebrain to regulate selective affiliation between adult mates, known as pair bond formation, as assessed by partner preference in the laboratory^{2, 3, 4}. The vasopressin V1a receptor (V1aR) is expressed at higher levels in the ventral forebrain of monogamous than in promiscuous vole species⁵, whereas dopamine receptor distribution is relatively conserved between species. Here we substantially increase partner preference formation in the socially promiscuous meadow vole by using viral vector V1aR gene transfer into the ventral forebrain. We show that a change in the expression of a single gene in the larger context of pre-existing genetic and neural circuits can profoundly alter social behaviour, providing a potential molecular mechanism for the rapid evolution of complex social behaviour.

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