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Marieta B. Heaton, Ph.D.

Contact Information:
Dr. Marieta B. Heaton, Director
Department of Neuroscience
University of Florida College of Medicine
Box 100244, McKnight Brain Institute
Gainesville, FL 32610-0244
Phone: (352) 392-1185
Fax: (352) 392-8347
Email: heaton@mbi.ufl.edu

Position:
Professor, Department of Neuroscience, University of Florida College of Medicine, Gainesville, FL; Director, Center for Addiction Research and Education, University of Florida.

Research Area:
Our research is focused on defining molecular mechanisms contributing to the devastating consequences of exposure to alcohol during nervous system development, which can lead to the fetal alcohol syndrome.

Training:
B.S., Florida State University; Ph.D., North Carolina State University (with Dr. Gilbert Gottlieb); Postdoctoral Fellowship, N.C. Department of Mental Health, Research Division (with Dr. Ronald W. Oppenheim).

Current Research:
Exposure to alcohol during development of the nervous system leads to a wide array of structural and functional abnormalities. Such exposure can lead to the fetal alcohol syndrome in human children. Our research is designed to improve the understanding of the specific molecular mechanisms underlying this anomalous development, with the goal of eventually developing strategies for therapeutic intervention to prevent or lessen these effects. Of particular interest in our studies are ethanol-induced alterations in survival-regulatory proteins (e.g., those of the Bcl-2 gene family), neurotrophic factors (e.g., NGF, BDNF), and oxidative processes (e.g., reactive oxygen species [ROS]; antioxidants). These studies are 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, neuronal cell culture, immunohistochemistry, stereological histological quantification, and ROS/antioxidant assays.

Recent Publications:
Heaton, M.B., Paiva, M. and Siler-Marsiglio, K. (2011) Ethanol influences on Bax translocation, mitochondrial membrane potential, and reactive oxygen species generation are modulated by vitamin E and brain-derived neurotrophic factor. Alcohol. Clin. Exp. Res., 35, 1122-1133.

Heaton, M.B., Paiva, M., Madorsky, I. and Shaw, G. (2006) The effect of bax deletion on ethanol sensitivity in the neonatal rat cerebellum. J. Neurobiol., 66, 95-101.

Siler-Marsiglio, K.I., Madorsky, I., Pan, Q., Paiva, M., Neeley, A.W., Shaw, G. and Heaton, M.B. (2006) Effects of acute ethanol exposure on regulatory mechanisms of Bcl-2-associated apoptosis promoter, Bad, in neonatal rat cerebellum: Differential effects during vulnerable and resistant developmental periods. Alcohol. Clin. Exp. Res., 30, 1031-1038.

Heaton, M.B., Madorsky, I., Paiva, M. and Siler, K.I. (2004) Vitamin E amelioration of ethanol neurotoxicity involves modulation of apoptotis-related protein levels in neonatal rat cerebellar granule cells. Devel. Brain Res., 150, 117-124.