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Department of Biology Faculty and Research |
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Department
Links W&L Links
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Education Undergraduate Degree: B.A, Univerisity of Illinois at Chicago, 1969 Graduate Degrees: M.S., Northwestern University, 1974 Ph.D., Northwestern University, 1977
Joined W&L Faculty in 1977
Courses Taught at W&L Fundamentals of Biology (Biology 111)
Biochemistry of the Cell (Biology 215)
Current
Research Interests
Maternal use of tobacco has been shown to have adverse effects on the
developing fetus. Evidence has linked tobacco use to sudden infant death
syndrome (SIDS), hyperactivity, low birth weight, perinatal disorders,
and spontaneous abortions. However, the precise role of nicotine in
these events, apart from the thousands of combustible products in
cigarette smoke (e.g. carbon monoxide, formaldehyde and lead), is
unclear, and nicotine replacement therapy has been proposed as a less
risky alternative to smoking. In an effort to provide basic biological
information on nicotine effects on developmental processes, as well as
to aid our understanding of normal central nervous system development,
my students and I investigate the effects of nicotine and other drugs on
neural development using the chick embryo as a model. Incubation of the chick embryo lasts twenty-one days, with each week
approximating the developmental processes of one human trimester. In our
experiments moderate doses of nicotine (similar to what a fetus
experiences if the mother smokes 3 cigarettes in a 30 minute period) are
applied to the embryo and the effects on a target structure, the
oculomotor nuclei (OMN) are assessed. The OMN are cranial nerves
composed entirely of motoneurons, which contain nicotinic cholinergic
receptors (binding both to acetylcholine and nicotine), and which
control most of the muscles that move the eyes. Using various
biochemical assays and in situ hybridization techniques, we have
determined that nicotine has a growth promoting effect on the OMN,
causing presumably inappropriately connected neurons to persist. We
provide evidence that nicotine acts to protect inappropriately connected
supernumerary neurons from the normal developmental process of selective
ablation by apoptosis ("cell suicide"), thereby resulting in
abnormally high neuronal activity in the offspring. In addition, the
neurons are larger than normal, suggesting the upregulation of nicotinic
receptors. We hypothesize that supernumerary neurons are a partial
biological explanation for hyperactivity disorders, perhaps due to
excess signal amplitude as a response to stimuli. Past studies in this laboratory determined the role of nicotine on
brain mitotic activity and its effect on the rate of OMN apoptosis.
Presently, we are determining the cholinergic receptor type found in
selected areas of the brain. It is our goal to provide basic biological
information which will be useful in understanding and/or preventing
hyperactivity disorders and other nicotine-related developmental
impairments.
Selected
Publications
(Asterisks denote student authors.)
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