Tracy L Bale
410F Hill Pavilion
380 S. University Ave.
Philadelphia, PA 19104
Philadelphia, PA 19104-4192
BS (Molecular biology/Genetics)
Washington State University, 1992.
University of Washington, 1997.
Description of Research ExpertiseKEY WORDS:
prenatal stress, maternal high fat diet, epigenetics, mouse model, neurodevelopmental disorders, depression, stress, sex differences, obesity, CRF, neuroendocrinology
Developing mouse models of stress sensitivity using genetic and prenatal manipulations to to understand the mechanism and heritability for increased susceptibility to neurodevelopmental disorders. Determine the molecular mechanisms by which stress factors influence appetite and reward. Examine the effects of maternal stress-sensitivity on fetal development and long-term physiological and behavioral responses.
Genetic mouse models for behavioral analyses including stress, anxiety, depression, feeding and reward models; gene expression and epigenetic identification by in situ hybridization, real-time PCR, PCR Arrays, ChIP, bisulfite sequencing; biochemistry using Western blot; molecular biology for gene detection; and plasma hormone detection using radioimmune assays.
Our research focuses on developing mouse models of stress sensitivity related to neurodevelopmental and neuropsychiatric disease. We utilize genetic and prenatal manipulations to elucidate mechanisms contributing to disease predisposition. We have focused on utilizing approaches that range from fetal antecedents in programming of long-term disease risk to genetic targeting of cell type specific knockout mice. We have focused on developing models of disease including affective disorders and obesity utilizing approaches that range from fetal antecedents, involved in programming of long-term disease risk, to genetic targeting of cell type specific knockouts. We have initiated multiple lines of investigation that will provide insight into the timing and sex specificity of early life events promoting disease susceptibility, the maturation of central pathways during key periods of development, and the epigenetic mechanisms involved in long-term effects following stress exposure.