Generally speaking, our work examines the intersection between neuroendocrine systems and neuroimmune function under a variety of circumstances. Ongoing studies test specific hypotheses regarding the overall impact of external threats such as stress challenges and binge-like alcohol exposure on specific features of brain function using rodent models. A long term goal of our work is to better understand developmental differences in, and long lasting consequences of, early life stress and alcohol exposure. More recently, our work has included growing emphasis on circuit-level changes that disrupt social behavior among aged populations. Our approach utilizes a combination of molecular procedures (RT-PCR, RNASeq), behavioral pharmacology, in vivo microdialysis and immunohistochemistry to achieve these goals.
Neurobiology of acute and chronic stress
Historically, the lab has focused on neuroendocrine and neuroimmune consequences of psychological stress challenges, with the over-arching goal of understanding how stress influences the development of neuropsychiatric conditions. Ongoing studies are exploring age-specific, early developmental vulnerabilities to the long-term impact of stress exposure, as well as circumstances and mechanisms that contribute to stress adaptation. We are particularly interested in the hypothalamic-pituitary-adrenal (HPA) axis due to its involvement in stress processes and as a key regulator of inflammation.
Alcohol - Neuroimmune Interactions
Alcohol use and abuse produces tell-tale signs of CNS inflammation. One of our main projects focuses on fluctuations in neuroimmune genes across cycles of intoxication and withdrawal. Interestingly, adolescents appear to be far less sensitive to the neuroimmune consequences of alcohol, yet binge-like alcohol exposure during adolescence produces long-lasting changes in neuroimmune function that persist into adulthood. Ongoing projects are exploring cellular and functional consequences of alcohol in early development and late aging using rodent models.
Natural aging and overall brain health
Late aging is associated with heightened inflammation in the CNS and elsewhere in the body. One of our projects examines interactions between neuroinflammation and the regulation of social behavior, hypothesizing that aging-related inflammation is responsible for short-circuiting the normal expression of social behavior and other aspects of neuroendocrine function, which are known to decline in aging individuals. The goal is to identify specific pathways to improve social motivation and engagement in late aging, since social interaction is highly predictive of quality of life in aged individuals.