SCoBIRC FACULTY

Mark Prendergast, Ph.D.

Associate Professor
Department of Psychology

Research Interests

My laboratory's research efforts are focused on examining mechanisms involved in brain damage, particularly in the rat hippocampus, that results from exposure to:

• alcohol
• HIV-1 proteins
• pesticides
• psychomotor stimulants

In studying these topics, my laboratory employs a broad range of neurochemical and behavioral techniques, including cell culture of brain tissue, in vivo rodent studies, and immunohistochemistry. To go to the lab webpage click here.

Representative Publications

Mulholland, P. J., Harris, B.R., Wilkins Jr., L. H., *Self, R. L., Blanchard II, J. A., Holley, R. C., Littleton, J. M., & Prendergast, M. A. (2003). Opposing effects of ethanol and nicotine on hippocampal calbindin-D 28K expression. Alcohol, 31(1-2), 1-10.

*Self, R. L., *Mulholland, P. J., Nath, A., Harris, B. R., & Prendergast, M. A. (2004). The human immunodeficiency virus type-1 transcription factor tat produces elevations in intracellular Ca2+ that require function of an N-methyl-D-aspartate receptor polyamine sensitive-site. Brain Research, 335(1), 39-45.

Prendergast, M. A., Harris, B. R., *Mulholland, P. J., Blanchard II, J. A., Gibson, D. A., Holley, R. C., & Littleton, J. M. (2004). Hippocampal CA1 region neurodegeneration produced by ethanol withdrawal requires activation of intrinsic polysynaptic hippocampal pathways and function of N-methyl-D-asparate receptors. Neuroscience, 124(4), 869-877.

*Mulholland, P. J., *Self, R. L., Harris, B. R., Littleton, J. M., & Prendergast, M. A. (2004). (-)Nicotine ameliorates corticosterone's potentiation of N-methyl-D-aspartate receptor-mediated CA1 toxicity. Neuroscience, 125(3), 671-682.

Prendergast, M. A. (2004). Do women possess a unique susceptibility to the neurotoxic effects of alcohol? Journal of the American Medical Womens Association, 59(3), 225-227.

*Mulholland, P. J., *Self, R. L., Harris, B. R., Littleton, J. M., & Prendergast, M. A. (2004). Choline exposure reduces potentiation of N-methyl-D-asparate toxicity by corticosterone in the developing hippocampus. Developmental Brain Research, 153(2), 203-211.

*Self, R. L., *Mulholland, P. J., Harris, B. R., Nath, A. & Prendergast, M. A. (2004). Cytotoxic effects of exposure to the human immunodeficiency virus type-1 protein tat in the hippocampus are enhanced by prior ethanol treatment. Alcoholism: Clinical and Experimental Research, 28(12), 1916-1024.

*Mulholland, P. J., *Self, R. L., Harris, B. R., Little H. J., LIttleton, J. M., & Prendergast, M. A. (2005). Corticosterone increases damage and cytosolic calcium accumulation associated with ethanol withdrawal in rat hippocampal slice cultures. Alcoholism: Clinical and Experimental Research, 29(5), 871-881.

*Mulholland, P. J., *Self, R. L., Stepanyan, T. D., Little, H. J., Littleton, J. M., & Prendergast, M. A. (2005). Thiamine deficiency in the pathogenesis of chronic ethanol-associated cerebellar damage in vitro. Neuroscience, 135(4), 1129-1139.

*Mulholland, P. J., Stepanyan, T. D., *Self, R. L., Hensley, A. K., Harris, R. R., Kowalski, A., Littleton, J. M., & Prendergast, M. A. (2005). Corticosterone and dexamethasone potentiate cytotoxicity associated with oxygen-glucose deprivation in organotypic cerebellar slice cultures. Neuroscience, 136, 259-267.

*Self, R. L., Smith, K. J., *Mulholland, P. J., & Prendergast, M. A., (2005). Ethanol exposure and withdrawal sensitizes the rat hippocampal CA1 pyramidal cell region to beta-amyloid (25-35)-inducted cytotoxicity: NMDA receptor involvement. Alcoholism: Clinical and Experimental Research, 29(11), 2063-2069.

*Student