Understanding social attachment: Molecular and genetic approaches to study the neural basis of social attachment throughout development and in disease

We study the function and developmental programming of the neural circuits that underlie social attachment, how they operate at different times in an animalís life to regulate social behaviors, and how early experience or genetic lesions that are associated with psychiatric illnesses alter these circuits to change social attachment behaviors. To model social attachment behaviors in the lab, we use prairie voles, which are monogamous rodents that form life-long pair bonds between mates. We have developed molecular genetic tools to both generate voles with specific mutations and to label and manipulate populations of neurons in the vole brain. Using these tools and comparative studies between prairie voles and closely related species with other patterns of social behaviors, we aim to understand the molecular, genetic, and neural basis of attachment.

Current projects:

1) What behaviors at early developmental stages correlate with pair bonding, and do shared neural mechanisms underlie social behavior at different developmental stages?

2) How does reward circuitry interact with the neural circuits that underlie social attachment to influence attachment behaviors, and how do such circuits evolve to reinforce distinct social behaviors in different species?

3) How do the circuits that mediate social development transform during development in response to developmental programs and environmental cues?

4) How are early social experiences encoded in the brain, and how does such experience affect the neural circuits that mediate social attachment and influence behavior later in life?

5) How do mutations associated with psychiatric illnesses such as autism spectrum disorder and schizophrenia, which often result in profound disruptions in social attachment, affect the circuits that mediate attachment to produce specific patterns of behavioral phenotypes, and what are the earliest behavioral or physiologic indications of dysfunction in these neurons?