Our work explores the interplay between genes and environment, with special emphasis on the importance of social relationships in modulating mood and behavior.
Investigating the role of candidate cis-regulatory variants in behavioral diversity
Differences in gene expression are thought to contribute to individual and species level differences in morphology and behavior. Despite numerous correlations between putative cis-regulatory variants and behavior, we still lack a fundamental understanding of genotype-phenotype relationships in the context of the mammalian brain. Our lab uses transgenic approaches to elucidate the specific contribution of cis-regulatory variants within the complex cellular environment of the brain. Our previous work has focused on an evolutionary question of how a polymorphism in the vole vasopressin 1a receptor gene promoter modulates expression of vasopressin receptor and monogamy-related behaviors. Our more recent efforts have transitioned to understanding how a common polymorphism in the human serotonin 1a receptor gene promoter contributes to risk for anxiety and depression. Our lab, along with collaborators at Emory University, Columbia University, and University of Mississippi found that this polymorphism is associated with increased risk for psychiatric hospitalization and suicide attempts. We have generated a mouse model of this allele, and our ongoing efforts are focused on using this model to understand the mechanisms underlying this gene-association.
Social modulation of mood and anxiety
Social relationships play a fundamental role in human health and well-being and can have an immediate effect on our mood. Positive social interactions reduce the behavioral, physiological, and neural response to stress or threat, a phenomenon referred to as social buffering. Social buffering can have profound effects – so much so that during World War II young children in London experienced less stress if they endured the blitz with their family than if they had previously evacuated to safety without them. Subsequent studies have linked strong social support with a decreased likelihood of developing mental illness and an enhanced ability to recover from heart attacks, cancer, and other illnesses. Recognition of the importance of social buffering led psychologists in the 1950s to suggest that for space-race astronauts, “stress response…could be held to a minimum by proper use of social stimuli.” My lab has taken a contemporary view of this approach; we are dedicated to identifying the neuromolecular mechanisms that mediate social buffering in order to identify novel therapeutic opportunities relevant to both mental and physical health.
The robust effects of companionship are highly conserved and have been documented in many species. New environments are less stressful for a goat kid if its mother is present, and groupmate presence blunts the stress-hormone response in monkeys exposed to a live snake. Thus, my lab has pioneered behavioral paradigms to assess social buffering in mice. Mice typically respond to a fearful environment by freezing, but we have found that the presence of a familiar companion mouse decreases freezing in threatening environments. Our ongoing work is focused on understanding the cellular basis of this phenomenon using novel transgenic tools, optogenetics, and sequencing-based approaches.
The making and breaking of pair bonds
Human social bonds are highly selective and complex, none more so than those that develop from romantic relationships. The biggest predictor of overall life satisfaction is one’s satisfaction with their spouse. The loss of such an individual can lead to profound grief and increased risk for mental and physical ailments. Unfortunately, commonly used laboratory rodents, such as mice and rats do not form highly selective bonds between adults, and cannot be used to study this essential facet of human behavior; instead our lab uses monogamous prairie voles. We use cutting-edge tools to visualize and manipulate the circuits that mediate pair bonding in prairie voles. This includes use of in vivo calcium imaging, optogenetic manipulations, and chemogenetic manipulations. This work is broadly designed to identify the neuroplasticity underlying bond formation and how a sudden loss of a loved one impacts these circuits.