Dr. Kravitz is an Investigator in the Eating and Addiction Section, Diabetes, Endocrinology, and Obesity Branch of the National Institute of Diabetes and Digestive and Kidney Diseases. His work focuses on the study of basal ganglia circuits and how their function changes in disease states such as obesity, addiction, and depression. Under normal conditions, the basal ganglia drives animals toward the selection of specific behavioral outcomes. Learning can bias this selection process toward specific behavior by altering synapses within and outside the basal ganglia. In extreme cases, these synaptic alterations can produce pathological behavioral selection, as in obesity or addiction. Using behavioral testing, optogenetics, and in vivo electrophysiology and optical measurements, the lab characterizes changes in behavior following learning in a feeding context and attempts to understand the neural correlates and causes of these changes in behavior.
See more of his work: Kravitz Lab
Jennifer Kern and Katherine Flynt are two speech-language pathologists at Duke University who work with many autistic children. They shared their insights into autism and its relationship to eating abnormalities!
Lawrence David is an Assistant Professor in GCB and the Department of Molecular Genetics & Microbiology. His Lab is particularly interested in how commensal microbes help resist, and ultimately respond to, colonization by human pathogens. An active area of research is the longitudinal study of cholera infections among residents of Dhaka, Bangladesh. Primary research questions include: Can enteric microbial communities predict an individual’s susceptibility to cholera? Why do bacterial ecological successions follow cholera infection? What long-term effects do infection and treatment have on commensal gut microbes? The David Lab is also broadly interested in developing new modeling and visualization tools for time-series of complex microbial communities, as well as exploring the ecology of human microbiota in the developing world.
See more of his work: David Lab
Dr. Scott Magness is an Associate Professor in the Department of Cell Biology at UNC. His research is focused on the basic biology of intestinal stem cells, the genes that control their behavior, and translational approaches to stem cell based therapies for human disease and injury of the intestine. Furthermore his research focuses on elucidating genetic mechanisms underlying stemness and developing translational models to establish a finer understanding of stem cell-driven regeneration dynamics in homeostasis and injury. Using a combination of genetic mouse models and micro-frabricated bioengineered platforms, Dr. Magness’ team is exploiting the self-renewal capacity and multipotency of ISCs to develop long-term ex vivo models of the intestine and colon with primary tissues. These biomimetic models offer new solutions for compound screening and cell-based therapies.
See more of his work: Magness Lab.
Dr. Jenna McHenry, Assistant Professor of Psychology and Neuroscience at Duke University, starting Fall 2018
Hormonal regulation of a hypothalamic social reward circuit
Dr. Jenna McHenry was recently hired as an Assistant Professor of Psychology and Neuroscience at Duke University starting Fall 2018. She is currently completing her post-doctoral fellowship at the University of North Carolina- Chapel Hill in Dr. Garret Stuber’s laboratory. Her post-doctoral work has focused on investigating the neural circuitry that links social and emotional processing within the brain. As evident in reproductive mood disorders such as post-partum depression and premenstrual dysphoric disorder, hormonal flux can cause affective disorders. Dr. McHenry’s post-doctoral work has focused on studying the neural circuits—specifically the circuits involving the medial preoptic area (mPOA)— that regulate hormone mediated reward programming and sex specific behavior. In work published in Nature Neuroscience in 2017, Dr. McHenry used in vivo two-photon imaging in awake mice to identify a subset of neurotensin-expressing mPOA neurons that interface with the ventral tegmental area (VTA) to form a socially engaged reward circuit. By recording from these neurons both at different times in the female reproductive cycle and after ovariectomy, she found this subset of neurons is steroid-responsive, indicating steroids modulate social encoding. As an extension of her post-doctoral work, Dr. McHenry’s central research question in her laboratory will be to understand how social processing neurons are intertwined with or embedded into positive and negative valence systems. Further, her lab will investigate the interplay between social and non-social reward circuits. Her lab will use a combination of advanced techniques including freely moving calcium imaging and optogenetics to investigate these questions. We look forward to the exciting research that Dr. McHenry will bring to Duke as a new faculty member.
See Dr. McHenry’s work here.
“Microbiome-immune crosstalk in neurodevelopmental disease”
Dr. John Lukens is an Assistant Professor at the University of Virginia. His research aims to understand how immunologic pathways and interactions contribute to neurodevelopmental diseases. During his talk, he focused on his lab’s work related to the microbiome-immune crosstalk influencing autism and multiple sclerosis. Significant research exists implicating the microbiome in the pathogenesis of autism spectrum disorders. Dr. Lukens and his team found that microbiome differences between Jackson and Taconic mice change the TH17 response and the expression of an autistic phenotype. Further, they showed microbiota transfer of the maternal microbiome of susceptible, Taconic mice induces autism susceptibility in Jackson mice. They then asked what metabolites are affected by changes in the microbiome. They found that Taconic dam’s injected with Poly-IC have increased IL-17a compared to Jackson mice. Inhibiting IL-17 in pregnant dams rescued the mice from an autistic phenotype. Further work will investigate additional metabolic mediators and identify protective commensal bacteria. Dr. Lukens then shared his work on inflammasome biology, specifically with relation to experimental autoimmune encephalomyelitis (EAE), a mouse model for multiple sclerosis. Caspase 1 in inflammasomes is thought to be required to cleave IL-1β into active IL-1. However, research from the Lukens lab suggests inflammasome-independent cleavage of IL-1 is important in driving EAE. They found that reduced levels of IL-1 receptor correlate with a reduced disease burden; knocking out caspase 1 does not confer protection, but knocking out the IL-1 receptor does. Further research will seek to better define the pathways and pharmaceutical targets involved in this phenomenon.
Check out Dr. Lukens’s work here: Lukens Lab