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Summer Undergraduate Research Fellowship Mentor

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Sandra M Mooney, Ph.D.

Assistant Professor, Neuroscience and Physiology
3210A Weiskotten Hall
Upstate Medical University
750 East Adams Street
Syracuse, NY 13210

Education and Clinical Training

Ph.D.: 1997, University of Otago, Dunedin, New Zealand

Research Program and Department Affiliations

Biomedical Sciences Program
Neuroscience Program
Neuroscience and Physiology
Physiology Program

Research Interests

Cell death and survival in the developing brain; Mechanisms of ethanol toxicity; models of fetal alcohol syndrome and autism.

Research Abstract

Early exposure to ethanol profoundly affects development of the nervous system. Indeed, fetal alcohol exposure has been described as the primary cause of mental retardation. During development, neurons are overproduced and a subset are eliminated during a period of naturally occurring neuronal death (NOND). NOND is the mechanism used to match projection and target populations within a system. Exposure to ethanol interferes with numerical matching in the trigeminal-somatosensory system. There are 33% fewer neurons in the principal sensory nucleus of the trigeminal nerve (PSN) and somatosensory cortex (2nd and 4th order neurons) in ethanol-treated rats. In contrast, the number of neurons in the thalamic ventrobasal nucleus (VB)(3rd order neurons) is not altered by ethanol. Neuronal survival results from the ability of young neurons to successfully compete for neurotrophin(s) (e.g., nerve growth factor) that are available in limited supply. Expression and activity of these factors is compromised by ethanol. One project in my lab tests the hypothesis that ethanol-induced disruption of neurotrophins underlies the changes in the trigeminal-somatosensory system. Two complementary models are used: in vivo experiments are used to examine the effect of ethanol on neurotrophin ligand and receptor expression, and in vitro studies using organotypic slice cultures are used to examine the effects of ethanol on expression and activation of neurotrophin receptors. These studies will (1) assess mechanisms by which ethanol disrupts trigeminal-somatosensory development, (2) provide valuable data on neurotrophin function, and (3) be a base for future mechanistic studies of the role of neurotrophins in development.

This profile was last updated on 09/29/2008

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