Marieta Heaton, Ph.D.
Director, Center for Addiction Research & Education (CARE)
Department of Neuroscience
University of Florida
1149 Newell Drive
PO Box 100244
Gainesville, FL 32611-0244
Office Phone: (352) 273-5094
Lab Phone: (352) 392-3390
|1966-1969||Predoctoral Traineeship||National Science Foundation|
|North Carolina Sate University
Raleigh, North Carolina
Key Words: Developmental Neurobiology, Fetal Alcohol Syndrome, Apoptosis, Ethanol Neurotoxicity
Consumption of alcohol during pregnancy can produce a wide array of morphological, neurological and behavioral abnormalities, known as fetal alcohol spectrum disorder (FASD), or the more severe, fetal alcohol syndrome (FAS). The anomalies associated with developmental alcohol exposure, such as hyperactivity, attention deficits, learning and memory difficulties, impaired motor abilities and lowered IQ, are debilitating and enduring. In spite of the awareness of the dangers of such consumption, many women drink during pregnancy, and the incidence of FAS/FASD in the United States is estimated to be as high as 1 in 100 births. Our research is focused on defining molecular mechanisms underlying FAS/FASD, with the aim of devising strategies to prevent or mitigate the devastating effects of alcohol on the developing nervous system.
Exposure to alcohol during development of the nervous system leads to a wide array of structural and functional abnormalities, with widespread loss of developing neurons. Such exposure can lead to Fetal Alcohol Spectrum Disorder or the more severe Fetal Alcohol Syndrome in human children. Research in our lab is focused on defining the molecular mechanisms underlying this anomalous development, with the goal of eventually devising therapeutic strategies to prevent or lessen these effects. Our recent studies are concerned with investigating (1) ethanol effects on expression and interactions of proteins of the survival-regulatory Bcl-2 gene family; and (2) the role of ethanol-induced disruption of the cellular redox state in these ethanol-mediated apoptotic processes. If a linkage between oxidative processes and alcohol-induced cell death can be established, it is possible that this linkage can be interrupted by therapeutic intervention. These studies are being carried out using fetal and neonatal rats, primary neuronal cultures, and transgenic and gene-deleted mice. Procedures in use include ELISA and Western blot protein assays, cell cultures, immunohistochemistry, stereological histological quantification, and ROS/antioxidant assays.