Behavioral Neuroscience Lab
Director: Timothy Moran, Ph.D.
Our overall research program is aimed at identifying the roles of various neural signaling pathways in the controls of food intake and body weight. The current research takes a number of approaches. The first involves the identification of the neural representation of meal-related satiety signals. Multiple feedback signaling pathways are activated by food ingestion and the gastrointestinal presence of digestion products. We are examining how signals from multiple sites and stimulus modalities are integrated within specific brain nuclei and, in an effort to model eating disorders, how alterations in feeding patterns can influence these neural representations.
The second approach involves the identification of interactions between peripheral, within-meal, satiety signals and hypothalamic peptide systems involved in overall energy balance. We are currently examining how the activity of hypothalamic leptin, NPY, CCK, CFR, CART and melanocortin systems interact with ascending satiety pathways to alter meal size. We are also investigating how alteration in cellular energy availability and production are transduced into changes in food intake and body weight. These experiments focus on the de novo fatty acid synthesis pathway in critical hypothalamic sites and take advantage of a novel group of chemicals that inhibit the production of fatty acids and/or stimulate fatty acid oxidation. We are examining how exercise not only increases energy expenditure but also reduces food intake. These experiments focus on the regulation of peptide gene expression in hypothalamic systems involved in energy balance.
Finally, we are examining how gestational factors can bias metabolic programming to contribute to altered feeding and obesity. Experiments are conducted at multiple levels and employ behavioral, physiological and molecular in vivo and in vitro paradigms.
Overweight and obesity is a growing public health problem worldwide, particularly among children. My current studies examine how environmental manipulations during development, specifically the intrauterine and early postnatal environments, influence the metabolic phenotype of the offspring. We are using a rat model to study the short- and long-term behavioral, neuroendocrine, and metabolic consequences of prenatal stress and changes in maternal nutrition.
Zachary A. Cordner, M.D., Ph.D.
Zachary A. Cordner, MD-PhD, is an Assistant Professor of Psychiatry & Behavioral Sciences at the Johns Hopkins University School of Medicine, and a faculty member of the Johns Hopkins Mood Disorders Center. Dr. Cordner completed his medical training, PhD, psychiatry residency, and chief residency at Johns Hopkins. He was also named an Alexander Wilson Schweizer Fellow in Mood Disorders at Johns Hopkins. Dr. Cordner has clinical expertise in the diagnosis and management of complex and difficult to treat mood disorders. As a physician-scientist and member of the multi-disciplinary Behavioral Neuroscience Lab, Dr. Cordner also utilizes a wide variety of behavioral, molecular, and cellular techniques to understand complex mechanisms underlying stress sensitivity and resilience – including consideration of factors such as sex differences, critical periods of stress exposure, and gene by environment interactions. Dr. Cordner also investigates treatments for stress-related psychiatric disorders, including several studies assessing the mechanisms of psychedelic drugs.
Kimberly R. Smith, Ph.D., M.S.
Chantelle Terrillion, Ph.D.
Instructor and Director of Behavioral Core
Lindsey K. Macias, M.S.
I am broadly interested in how diet, nutrition, and environmental stressors alter gut microbiota composition and ultimately influence behavior and metabolism. My current thesis work looks at the effects of maternal consumption of high-fat (HF) diet specifically during gestation and lactation on offspring gut-brain-axis development in rodent models. There are two main aspects to my research: one focusing on gut development and intestinal satiety hormone signaling in maternal high fat diet offspring, and the other focusing on neurodevelopment and cognitive function after exposure to maternal high fat diet. Despite HF offspring being weaned onto a low-fat diet, they continue to display lasting cognitive deficits as well as decreased expression of small intestinal satiety peptides (Cck, Gcg, Pyy) in adulthood. My data suggest that this may be due to increased levels of systemic inflammation (CRP, IL-1b) also present during this critical developmental period. I am currently exploring possible interventions to manipulate gut microbiome composition in order to dampen or prevent systemic inflammation, which may be contributing to these phenotypes.
Brianna Bullock, B.S.