Joined W&L Faculty in 1977
Graduate Degrees: M.S., Northwestern University, 1974
Ph.D., Northwestern University, 1977
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.
J.J. Wielgus, L. C. Downey*, K.W. Ewald*, M.E. Hatley*, K.C. Wilson* and R.H. Yeilding*. Exposure to low concentrations of nicotine during cranial nerve development inhibits apoptosis and causes cellular hypertrophy in the ventral oculomotor nuclei of the chick embryo. Brain Research 1000: 123-133 (2004).
J.J. Wielgus, L.B. Aden* and R.M. Franks*. Site of synthesis and phylogenetic distribution of a hemolymph trophic factor of the tobacco hornworm, Manduca sexta. In Vitro Cellular and Developmental Biology 30A: 696-701 (1994).
J.J. Wielgus, L.B. Aden* and R.M. Franks*. Characterization and site of synthesis of a hemolymph trophic factor in the tobacco hornworm, Manduca sexta. In Vitro Cellular & Developmental Biology 29A: 31A (1993)
J.J. Wielgus, G.A. Caldwell*, R.L. Nichols* and C.F White*. Purification, properties, and titer of a hemolymph trophic factor in larvae and pupae of Manduca sexta. Insect Biochemistry 20: 65-72 (1990).
J.J. Wielgus. Stimulation of intermoult cuticle deposition by a haemolymph trophic factor in the tobacco hornworm, Manduca sexta. Insect Biochemistry 13:313-322 (1983).
J.J. Wielgus, W.E. Bollenbacher and L.I. Gilbert. Correlations between epidermal DNA synthesis and haemolymph ecdysteroid titre during the last larval instar of the tobacco hornworm, Manduca sexta. J. Insect Physiol. 25: 9-16 (1979).
W.E. Bollenbacher, S.L. Smith, J.J. Wielgus and L.I. Gilbert. Evidence for an α-ecdysone cytochrome p-450 mixed function oxidase in insect fat body mitochondria. Nature 268: 660-663 (1977).