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Dr. Mary E. Blue is a research scientist in the Neuroscience Laboratory at Kennedy Krieger Institute. She is also an associate professor, Department of Neurology and Neuroscience, at Johns Hopkins University School of Medicine.
Biographical Sketch:
Dr. Blue received her B.A. cum laude in Biology and Art from Cornell College in Mount Vernon, Iowa in 1977. She received her Ph.D. from the Department of Cell Biology at the University of Texas Health Science Center at Dallas in Dallas, TX in 1982. Dr. Blue continued her career as a postdoctoral fellow in the Department of Cell Biology and Neuroscience at Johns Hopkins University School of Medicine in Baltimore, MD between 1982-1989 and has continued as research scientist at Kennedy krieger Institute from 1989 until the present. Dr. Blue acted as assistant professor in the Department of Neurology at Johns Hopkins University School of Medicine from 1992-1999. She continues as associate professor in the Department of Neurology since 2000 and serves as associate professor in the Johns Hopkins University School of Medicine, Department of Neuroscience as well.
Research Summary:
Neurotransmitter Mechanisms in Development and Activity-Dependent Plasticity
The research in Dr. Blue's lab examines the roles neurotransmitters play as trophic agents in cortical development and plasticity. This research has demonstrated that monoaminergic and glutamatergic neurotransmitter systems are both altered by and influence injury in neonatal and adult hypoxia-ischemia animal models and in specific developmental disorders such as Down syndrome, autism and Rett syndrome (both in postmortem tissue and in animal models).
Activity-dependent plasticity plays an important role in the "sculpting" of synaptic connections in the postnatal human cerebral cortex and in the "reassignment" of cortex during recovery after early brain injuries. These plasticity studies focus on mechanisms by which cerebral cortex is influenced by peripheral stimuli and by which function is reassigned from one area of brain to another after neonatal injury. To study these mechanisms the rodent whisker-to-barrel system is used as a model of cortical plasticity. Rats and mice use their whiskers to navigate in their world and a precise "map" of the rodent face and whiskers is relayed through the brain to the cerebral cortex. Specialized anatomical configurations called "barrels" structurally and functionally linked to individual whiskers. Much like the reorganization of the human cortex after amputation, peripheral injury resulting from ablation of a single whisker follicle produces atrophy of the cortical barrel connected to it, and enhanced growth of surrounding barrels. These results suggest that glutamate receptors appear to mediate activity-dependent enlargement of some barrels and retraction of others in response to whisker clipping. Other studies have shown that neurotransmitter-specific afferents to the cortex (including acetylcholine-containing axons from the nucleus basalis) influence the degree of cortical plasticity. This model has also been used to investigate the effects of lead on the developing cortex. Lead poisoning in young children causes permanent loss of intelligence and remains common among poor urban children. Approximately 5% of the children tested in Baltimore from 1996 to 1998 suffered lead poisoning (blood lead greater than 20 g/dl). Studies underway in collaboration with Drs. Mary Ann Wilson, Michael V. Johnston and Gary W. Goldstein at the Kennedy Krieger Institute indicate that that low levels of lead exposure, comparable to those seen in many impoverished urban children, cause structural alterations in the developing barrel fields. This may involve the impact of lead on activity-dependent plasticity by increasing "synaptic noise" at glutamate receptors.
Recent Publications/Presentations:
Blue, M.E., S. Naidu and M.V. Johnston. Altered development of amino acid receptors in frontal cortex from girls with Rett syndrome. Ann. Neurol. 45:541-545, 1999.
Lange, M.S. M.V. Johnston, E.E. Tseng, W.A. Baumgartner, and M.E. Blue. Apoptosis detection in brain using low magnification darkfield microscopy. Exp. Neurol. 158: 254-260, 1999.
Wilson, M.A., M.V. Johnston, G.W. Goldstein, and M.E. Blue. Neonatal lead exposure impairs development of rodent barrel field cortex. Proc. Natl. Acad. Sci., 97:5540-5545, 2000.
Blue, M.E. and M.V. Johnston. Amino acid receptor studies in Rett syndrome. In Rett Disorder and the Developing Brain. A. Kerr and I.W. Engerstrom Eds. Oxford: Oxford University Press pgs. 115-118, 2001.
Johnston, M.V., A. Nishimura, K. Harum, J. Pekar and M.E. Blue. Sculpting the developing brain. Adv Pediatr. 48:1-38, 2001.
Purcell, A.E., O.-H. Jeon, A.W. Zimmerman, A.M., M.E. Blue and J. Pevsner. Postmortem abnormalities of the glutamate neurotransmitter system in autism. Neurology. 57:1618-1628, 2001.
Donovan, S.L., L.A. Mamounas, L.A. Andrews, A.M., M.E. Blue and J.S. McCasland. GAP-43 is critical for serotonergic ingrowth and arborization in mouse forebrain. J Neurosci. 22:3543-3552, 2002. | 